Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
112 Cards in this Set
- Front
- Back
|
pre-requisites for normal PaO2 |
-normal PA02 -good diffusion -appropriate V/Q ratio |
|
|
pre-requisites for normal O2 delivery |
-mostly depends on Hb saturation not dissolved O2 -also depends on cardiac output -factors that alter Hb binding curve: oxidation state, pH, pCO2, Temp, 2,3-DPG levels |
|
|
causes of low PaO2 w/ normal A-a gradient |
-decreased FiO2 -hypoventilation |
|
|
causes of low PaO2 w/ high A-a gradient |
-thickened diffusion barrier -V/Q mismatch (low ratio-->hypoxemia) -Right to left shunts |
|
|
alveolar gas equation |
PAO2=FiO2(Pb-Ph2o)-PaCO2/R
R=~.8 Pb-Ph20=~713 |
|
|
Hypoxia vs hypoxemia |
hypoxemia= blood oxygenation eg. CaO2, PaO2, or SaO2
Hypoxia= inadequate tissue oxygenation |
|
|
lung acinus |
a respiratory bronchiole + alveolar duct + alveoli |
|
|
obstructive airway disease |
= increased resistance to air flow
major diseases: Emphysema Chronic bronchitis Bronchiectasis Asthma |
|
|
restrictive lung disease |
= reduced expansion of lung parenchyma
eg. pulmonary fibrosis
|
|
|
emphysema definition |
-enlargement of distal airways-->destruction of alveolar walls w/o fibrosis -four patterns: centriacinar, panacinar, paraseptal, irregular |
|
|
centriacinar emphysema |
-95% of emphysema cases -affects respiratory bronchioles -most prominent in upper lobes -associated w/ smoking -lungs not voluminous |
|
|
panacinar emphysema |
-acini distal to respiratory bronchiole affected -mostly lower lobes -associated w/ alpha 1-antitrypsin deficiency -voluminous lungs |
|
|
chronic bronchitis |
-persistant productive cough for > 3mo's in 2 consecutive yrs -associated with inhaled irritants like tobacco features: -hypertrophy of bronchial SM mucus glands -increased goblet cells -mucus plugging -chronic inflammation w/ fibrosis -may be exacerbated by secondary infection |
|
|
Reid index |
the ratio of thickness of the bronchial mucus glands to the thickness of the wall
(normal=0.4, much higher in chronic bronchitis) |
|
|
bronchiectasis |
-dilation of the bronchi/bronchioles due to destruction of the wall -results from infection/CF/bronchial obstruction -affects lower lobes -can see intense acute and chronic inflammation, ulceration, squamous metaplasia and fibrosis |
|
|
asthma pathology |
-distended lungs -mucus plugs w/ curshmann spirals and charcot leyden crystals -edema/inflammation esp. eosinophils -hypertrophy of mucus glands and bronchial smooth muscle |
|
|
4 stages of pneumonia inflammation |
congestion red hepatization gray hepatization resolution |
|
|
4 complications of pneumonia |
-necrosis-->abscesses -pleuritis/empyema -fibrosis -bacterial dissemination |
|
|
histology of bacterial pnuemonia |
-usually see lobar consolidation -fibrinopurulent exudate in the alveoli -or can present as bronchopneumonia: patchy pattern of suppurative inflammation in the bronchi and bronchioles |
|
|
viral pneumonia histology |
-interstitial inflammation w/ mononuclear infiltrates and lymphocytes -fibrous exudate can be seen--> hyaline membranes |
|
|
asthma definition |
-chronic inflammation of the airways -Eo's, mast, T cells play a role -obstructive disease (partly reversible) -hyperreactive airways -episodes of wheezing, SOB, tightness, and cough
|
|
|
chronic bronchitis etiology |
-highly associated w/ smoking -repeated irritation of the bronchi causes significant increase in mucus cells and glands -excess mucus impairs muco-ciliary clearance and can result in difficult to irradicate infection |
|
|
advanced chronic bronchitis |
-may develop bronchiectasis also -cyanosis and hypoxemia--> clubbing and cor pulmonale -may have hemoptysis and infections |
|
|
chronic bronchitis spirometry |
-reduced flow rates due to high airway resistance -low FEV1, FVC and ratio -normal diffusion unless complicated by bronchiectasis |
|
|
COPD underlying conditions |
-can be a combination of chronic bronchitis emphysema and asthma all causing airway obstruction in addition to other complications |
|
|
causes of airflow limitations in emphysema |
-expiratory collapse of distal airway -air trapping -hyperinflation |
|
|
chronic bronchitis vs emphysema PFTs? ABGs? CXRs? PE? |
PFTs: E=high RV / low DLCO not seen in CB ABGs: E=may be normal CB=usually hypoxemia CXRs: E=hyperaeration not seen in CB PE: E=barrel chest, resonance, pursed lips CB=productive cough, cor pulmonale, ronchi |
|
|
FEV1 |
-volume of air exhaled in the first second of a FVC test -abnormal if <80% predicted -indicative of large airway obstruction |
|
|
FVC |
-volume of air exhaled w/ maximal effort after full inspiration -abnormal if <80% |
|
|
FEF 25-75 |
-forced expiratory flow rate between 25-75% of FVC -largely effort independent -abnormal if <65% -reflects small airway obstruction (often an early indicator) |
|
|
FRC |
-is the amount of air still in the lungs after expiration during normal tidal breathing -measured by dilution or plethysmography |
|
|
RV |
-volume of air remaining in the lungs after a forced expiration -calculated by FRC-ERV |
|
|
TLC |
-total lung capacity= maximal volume of air |
|
|
DLCO |
-diffusion capacity of carbon monoxide
|
|
|
PFT obstructive pattern |
low: FEV1, FEV1/FVC ratio high: FRC, RV, sometimes TLC normal: FVC |
|
|
PFT restrictive pattern |
low: FVC, FEV1, FRC, TLC, RV normal-high: FEV1/FVC ratio |
|
|
diseases w/ obstructive PFT pattern |
-COPD, asthma, chronic bronchitis -fixed, variable intrathoracic, variable extrathoracic- upper airway obstruction |
|
|
diseases w/ restrictive PFT pattern |
-pulmonary fibrosis, kyphoscoliosis, neuromuscular disease, obesity, hypersensitivity pneumonitis (need both spirometry and volumes!) |
|
|
lung complaince |
-change in vol./change in pressure -depicted by pressure-volume curve -emphysema increases compliance (upshift) -fibrosis decreases compliance (downshift) |
|
|
FEV1/FVC ratio |
-abnormal <70% -indicates obstruction |
|
|
Uusual Interstitial Pneumonia (UIP) pathology |
-a histologic pattern associated w/ IPF -repeated injury and excessive fibrosis find: fibroblastic foci, temporal heterogeneity of lesions, increased septa, patchy honeycombing, subpleural/bibasilar reticular abnormalities |
|
|
Idiopathic Pulmonary Fibrosis (IPF) |
-a syndrome w/ pathology of UIP -excluded all known possible causes -clinically: older pts, slowly progressive SOB and non-productive cough, rales, clubbing, poor prognosis |
|
|
Non-Specific Interstitial Pneumonia (NSIP) pathology |
-dyspnea over several mo's, cough and fatigue -diffuse bibasilar opacification -temporally homogenous* -mild fibrosis* -responds to steroids* -younger pts*
|
|
|
Desquamative Interstitial Pneumonia (DIP) pathology |
-associated w/ smoking -alveoli filled w/ pigmented macro's -inflammatory cells in alveolar wall -good prognosis w/ quit smoking and steroids |
|
|
Hypersensitivity Pneumonitis (HP) pathology |
-exposure to environments antigens/dusts esp birds-->allergic alveolitis -leads to non-caseating granulomas -see plasma/lymphs + macro's -bronchiolitis and some interstitial fibrosis |
|
|
sarcoidosis pathology |
-systemic disease often affecting the lungs -causes non-caseating granulomas along broncho-vascular complexes -associated w/ varying degrees of hyalinization and fibrosis |
|
|
coal worker's pneumoconiosis pathology |
-anthracosis (carbon pigment in macro's) -'simple'=nodules w/ fibrosis adjacent to bronchioles -'complicated'= large black scars w/ dense fibrosis |
|
|
silicosis pathology |
-most prevalent chronic occupational disease -sandblasting, foundries, stone cutting, mining -mostly in upper zones forms large scars w/ massive fibrosis |
|
|
sings and symptoms of sarcoid |
-SOB, cough -skin, eyes, nodes, liver, spleen, bone, renal, CNS, arthritis -lofgren syndrome=arthritis, uveitis, fever, erythema nodosum on legs-->good prognosis |
|
|
radiology of sarcoid |
-90% have pulmonary involvement -CXR+HRCT stage I: bilateral hilar lymph's (BHL) only stage II: BHL + lung involvement stage III: lung involvement, no BHL Stage IV: lung fibrosis |
|
|
PFTs in sarcoid |
-decreased DLCO, TLC, FVC -restrictive pattern but can show signs of obstruction w/ endobrachial involvement |
|
|
pathogenesis of sarcoidosis |
-TB or berylliosis like rxn -immune mediated response to antigen -antigen transported to lymph nodes--> immune response and walling off of antigen--> granulomas |
|
|
treatment of sarcoid |
-goal is to prevent possible fibrosis -most cases spontaneously remit -treat pts w/ progression over 3-6 mo's, ocular, cardiac, or CNS involvement -treat w/ oral prednisone for ~1yr then taper, if relapse occurs add methotrexate, plaquenil or infliximab |
|
|
clinical presentation of silicosis |
-can be acute (wks-yrs post exposure)--> cough, fatigue, weight loss, pleuritic pain, crackles and rapid deterioration/respiratory failure w/in 5 yrs -mostly chronic (10-30 yrs post exposure)-->cough and dyspnea on exertion, mixed obstructive and restrictive PFT pattern, increases risk for TB and lung cancer
|
|
|
treatment options for HP, and pneumoconiosis |
-HP pts must avoid antigen and steroids may initially speed recovery -silicosis pts may get steroids/bronchodilators and tx for complicating infections -asbestosis pts must stop smoking, be screened for malignancies, get oxygen, prevent/treat any complicating infections |
|
|
mechanism of immune impairment |
-neutrophils: functional impairment or reduced numbers -T-cells: CD4 or CD8 -Splenectomy/B-cells: weak Ab response and susceptibility to encapsulated organisms -Barrier compromise -disease specific causes |
|
|
hospital acquired bacteria |
pseudomonas, ESBL, MRSA |
|
|
HIV pneumonia risks |
bacterial, PCP, and CMV at very low CD4 counts |
|
|
Steroid pneumonia risk |
bacterial, PCP, Aspergillus |
|
|
organ transplant pneumonia risk |
CMV |
|
|
pre-transplant serology |
-can predict the recipients risk for certain pathogens |
|
|
risks over time post transplant |
<1 month= donor derived bacteria, recurrent, or post op infection (not related to immunosuppression) 1-6 mo's=PCP, CMV, Fungi, TB, protozoa >6 mo's= Bacterial, CMV, influenza, RSV |
|
|
bone marrow engraftment |
occurs @ ~1 mo post transplant -risk shifts from bacteria, fungi, Toxo--> viruses like CMV, parainfluenza, RSV, HSV, also TB |
|
|
diagnosis of pneumonia in immunocompromised |
-CXR + probable CT -sputum analysis and often bronchoscopy for organism ID -treat empirically based on presentation and immune status |
|
|
progression of bacterial infection of CF pts |
MSSA/MRSA--> gram- (H.flu, Klebs) -->pseudomonas --> burkholderia |
|
|
Obstructive sleep apnea epidemiology
|
-OSA (5+ apneas/hour) affects ~25% of adult males and ~10% of females
-OSA syndrome (OSA + severe daytime sleepiness) affects 4% of adult males and 2% of females -associated w/ age, sex, obesity |
|
|
Constitutional symptoms of TB
|
- fever, night sweats, weight loss, anorexia, fatigue (cough hemoptysis also common)
|
|
|
PPD testing
|
-Intradermal injection of purified TB proteins
-interpretation depends on risk: >5mm= + for pts w/ immunodeficiencies, close TB contact, positive old CXR >10 mm= + for high incidence group or recent TST converter >15mm= + for those w\ no risk |
|
|
Interferon gamma release assays
|
-ex's: QFT-GIT or T-spotTB
-more specific than PPD - no good data about sensitivity -concern about pop's without the ability to make IFN gamma |
|
|
OSA pathogenesis
|
Recurring upper airway closure causes apnea episodes during sleep that last more than 10 secs and are associated with CVD, hypoventilation and excessive sleepiness
|
|
|
Diagnosis of OSA
|
-clinical findings + sleep study
-episodes of apnea w/ muscle activity -AHI=apneas/hyopapneas per hour (5-15=mild, 15-30=moderate, 30+ severe) |
|
|
OSA treatment
|
-lose weight!
- sleep hygiene -CPAP -surgery (tonsillectomy/UPPP) may relieve crowding of pharynx esp in children -mouth piece -O2 |
|
|
Central sleep apnea
|
- cheyne-stokes respiration
-crescendo-decrescendo breathing -caused by abnormal feedback from respiratory center due to circulatory delay - most common in advanced CHF -other causes exist* |
|
|
Sleep related hypoventilation
|
-primary (ondines curse): absent chemoresponsiveness but intact voluntary resp. Control assc. W/ phox2b mutation
-secondary (mechanical): eg. Obesity related hypoventilation sybdrome |
|
|
TB transmission
|
Most common route in the US is respiratory droplets and requires prolonged exposure in a poorly ventilated space
|
|
|
Factors that facilitate TB spread
|
Crowded living conditions, a population with little resistance and the virulence if the pathogen
|
|
|
Stages of TB infection
|
-primary: mycobacteria taken up by alveolar macros and divide/spread via lymphatics or blood usually--> containment in granulomas
-latency: bacteria alter their metabolism and lay dormant in the granulomas (10% progress/reactivity) -active/reactivated |
|
|
HIV and TB
|
T-cell immune response is required for granulomas formation and so dual infection leads to substantial risk of active TB
|
|
|
Obstructive sleep apnea epidemiology
|
-OSA (5+ apneas/hour) affects ~25% of adult males and ~10% of females
-OSA syndrome (OSA + severe daytime sleepiness) affects 4% of adult males and 2% of females -associated w/ age, sex, obesity |
|
|
Constitutional symptoms of TB
|
- fever, night sweats, weight loss, anorexia, fatigue (cough hemoptysis also common)
|
|
|
PPD testing
|
-Intradermal injection of purified TB proteins
-interpretation depends on risk: >5mm= + for pts w/ immunodeficiencies, close TB contact, positive old CXR >10 mm= + for high incidence group or recent TST converter >15mm= + for those w\ no risk |
|
|
Interferon gamma release assays
|
-ex's: QFT-GIT or T-spotTB
-more specific than PPD - no good data about sensitivity -concern about pop's without the ability to make IFN gamma |
|
|
OSA pathogenesis
|
Recurring upper airway closure causes apnea episodes during sleep that last more than 10 secs and are associated with CVD, hypoventilation and excessive sleepiness
|
|
|
Diagnosis of OSA
|
-clinical findings + sleep study
-episodes of apnea w/ muscle activity -AHI=apneas/hyopapneas per hour (5-15=mild, 15-30=moderate, 30+ severe) |
|
|
OSA treatment
|
-lose weight!
- sleep hygiene -CPAP -surgery (tonsillectomy/UPPP) may relieve crowding of pharynx esp in children -mouth piece -O2 |
|
|
Central sleep apnea
|
- cheyne-stokes respiration
-crescendo-decrescendo breathing -caused by abnormal feedback from respiratory center due to circulatory delay - most common in advanced CHF -other causes exist* |
|
|
Sleep related hypoventilation
|
-primary (ondines curse): absent chemoresponsiveness but intact voluntary resp. Control assc. W/ phox2b mutation
-secondary (mechanical): eg. Obesity related hypoventilation sybdrome |
|
|
TB transmission
|
Most common route in the US is respiratory droplets and requires prolonged exposure in a poorly ventilated space
|
|
|
Factors that facilitate TB spread
|
Crowded living conditions, a population with little resistance and the virulence if the pathogen
|
|
|
Stages of TB infection
|
-primary: mycobacteria taken up by alveolar macros and divide/spread via lymphatics or blood usually--> containment in granulomas
-latency: bacteria alter their metabolism and lay dormant in the granulomas (10% progress/reactivity) -active/reactivated |
|
|
HIV and TB |
T-cell immune response is required for granulomas formation and so dual infection leads to substantial risk of active TB |
|
|
bronchiolitis |
-often caused by RSV or para-flu 3 -occurs 4-6 after URI prodrome w/ inflammation--> obstruction and mucus -occurs mostly in infants -managed w/ O2, bronchodilators, steroids + other supportive care |
|
|
croup |
-commonly caused by para-flu 1/2 -1-2 day URI prodrome-->seal bark cough and inspiratory stridor -steeple sign on xray -manage w/ air humidification, epinephrine in complications |
|
|
Indicators for hospitalizing pneumonia pts
|
CURB-65: confusion, uremia, respiratory rate, low blood pressure, older than 65
|
|
|
Criteria for ICU admission in pneumonia pts
|
Major: respiratory failure or septic shock
Minor (>3): RR, PaO2/FiO2 < 250, multi-lobe, confusion, BUN>20, leukopenia, thrombocytopenia, hypothermia, hypotension, (pH<7.3) |
|
|
Diagnostic work up for Pneumonia
|
-PE w/ pulse-ox, CXR, usually a blood culture, sputum culture, and pneumococcal urinary antigen
-special cases: bronchoscopy/endotracheal culture in ICU pts, fungal and TB cultures w/ cavity infiltrates, thoracocentesis+culture w/ pleural effusion, legionella urinary antigen in suspected cases |
|
|
Solitary pulmonary nodule definition
|
- a lone opacity surrounded by normal lung parenchyma
- Btwn 3cm and 8mm |
|
|
Treatment of PE
|
-low molecular weight heparin is first line
-unfractionated heparin is first line for hemodynamically unstable pts -can also use thrombin inhibitors if heparin is contraindicated -warfarin for long term -thrombolytics for acute massive PE (no great evidence) -vena cava basket in pts w/ anticoagulant contraindications - embolectomy is rare |
|
|
PE prophylaxis
|
-external pneumatic leg compression
-heparin -warfarin |
|
|
Chronic thromboembolic pulmonary disease
|
Chronic failure of the fibrinolytic system leading to pulmonary hypertension and Cor pulmonale and must be treated surgically
|
|
|
Clinical characteristics pointing to malignant spn
|
-pt age >60
-smoker - hemoptysis -previous cancer of any kind |
|
|
CT scan characteristic of a malignant spn
|
-size: esp. > 2cm
-borders: esp. Irregular, lobulated, or spiculated -morphology: ground glass is worse -upper lobe -cavitated lesion w/ wall >15mm |
|
|
Causes of benign SPNs
|
-most often granulomatous (ie. TB, histo, coccidio, abscess, PCP, aspergillus, wegener's)
-less often soft tissue (eg. Hamartoma) or vascular malformation |
|
|
3 major risk factor for PE
|
Virchows triad
1) stasis of blood 2) change in coagulation state 3) trauma to vessel walls |
|
|
Sources of pulmonary emboli
|
Iliac-pelvic veins, femoral veins, calf veins
|
|
|
Physiological consequences of PE
|
-respiratory: increase in dead space, increase in minute and alveolar ventilation, shunting
-cardiac: arrhythmia esp. Tachycardia, pulmonary hypertension, low cardiac output, hypotension -other: hypothermia, cyanosis, altered mental status, low urine output |
|
|
Signs and symptoms of PE
|
-dyspnea, pleuritic pain, apprehension, hemoptysis, leg swelling at source
-tachycardia, pleural effusion, fever, elevated JVD |
|
|
Wells criteria
|
Symptoms of DVT- 3 pts
Other diagnosis less likely- 3 pts Heart rate >100- 1.5 pts Immobilization >3 days- 1.5 pts Previous DVT/PE- 1.5 pts Hemoptysis- 1 pt Malignancy- 1 pt <2= low risk 2-6 = moderate risk, do CTPA >6 = severe risk, treat |
|
|
Tests for PE
|
-ABG: rules out PE if no A-a gradient
-D dimer: rules out PE if normal -EKG: usually non-specific unless rare but classic S1,Q3,T3 is seen -Doppler: finding of DVT is specific but not sensitive -V/Q study: rules out PE if normal -CTPA- most commonly used, filling defect is diagnostic |
|
|
Cause of edema in acute lung injury
|
Damage to the alveolar walls increases the permeability and allows fluid to leak into the airspaces
|
|
|
Causes of ARDS
|
Shock/sepsis, infection, trauma, aspiration, drugs, inhaled toxins, DIC, pancreatitis, uremia, radiation, emboli
|
|
|
Mechanism of hypoxemia in ARDS
|
- alveolar effusion degrades surfactant leading to atelectasis and shunting
-PEEP can help alleviate this effect |
