Pulmonary
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| How does O2 from the air get into the tissues and CO2 from the tissues get in the air? | 1. A pump (non-tissue level, needs PFTs to measure); 2. Gas Exchange (mainly by diffusion, need blood gases and diffusion capacity to measure)
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| Volumes that can't be measured by spirometry: | total lung capacity, functional residual capacity, residual volume
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| Volumes that CAN be measured by spirometry: | tidal volume, vital capacity
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| Functional Residual Capacity (FRC) depends on: | chest wall and lung compliance
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| Negative pressure breathing | on inspiration, the dome-shaped diaphragm contracts, the abdominal contents are forced down and forward, and rib cage widens to inc vol of thorax; Forced expiration contracts abdom mm and pushes diaphragm up; intercostal-rib-vertebrae motions
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| Inspiration: active phase | process of taking air into lungs; ventilation d/t muscle contraction (diaphragm/intercostals) to inc thoracic cavity vol and *decrease intra-alveolar pressure so air flows into lungs*
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| Expiration: passive phase | letting air out of lungs d/t relaxation of diaphragm and elastic recoil of tissues to dec thoracic vol and inc intraalveolar pressure
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| Gas exchange: just some numbers | 300 million alveoli, 85 sq meters; volume of 4 liters
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| Anatomy of airways: conducting - 16 generations | no alveoli (*no gas exchange*); anatomical dead space; volume = 150mL; "bulk flow"
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| Anatomy of airways; Respiratory Zones - 7 generations | gas exchange; volume = 3L; "diffusion"
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| Pulmonary Capillaries | blood from R heart goes to lung; capillary diameter = 10um; thickness of blood-gas barrier = 0.3um; blood spends 3/4 sec in capillaries
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| O2 Physiology: Henry's Law | amount of O2 dissolved is proportional to the partial pressure of the gas above the solution
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| Two options for O2 in human blood when alveolar PO2 is 100 | 1. O2 dissolved in plasma (for each 1mmHg of PO2, there's .003mL O2 in 100mL blood (.3mL O2/100mL blood); 2. O2 bound to hemoglobin (1gm of Hb can hold 1.39mL O2; 1.39x15g of Hb/100mL = 21mL O2/100mL blood)
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| O2 Capacity | the amount of O2 bound to hemoglobin; ex: 1.39x15 = 21mL O2/100mL blood; carrying capacity gets reduced as hemoglobin gets reduced
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| O2 Saturation | % saturated = O2 bound to Hb divided by O2 capacity times 100
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| O2 Delivery | = CO x O2 content; [(HR x SV) x 1.39 x Hb x %Sat + (.003xPO2)]
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| Factors affecting O2 transport | shifting the O2 saturation curve to the right: increased temp, inc 2,3-DPG (chronic hypoxemia), inc PCO2, dec pH; hemoglobin concentration-anemia or polycythemia; carbon monoxide, PO2, cardiac output
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| Effect of shift of oxyhemoglobin curve to the right | affinity of hemoglobin for O2 is decreased; increased P50; increases O2 release at tissue level
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| Alveolar gas equation (what is the partial pressure of oxygen in the air)? | = 760 - 47 x .21 = 150mmHg; (760 = sea level barometric pressure at 37C; 47 is water vapor pressure; .21 is % of O2 in air)
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| Alveolar gas equation (what is partial pressure of oxygen in the alveoli?) | PAO2 = 760 - 47 x .21 - PACO2/R = 100mmHg; (PACO2 = 40mmHg, R = respiratory quotient = CO2 production/O2 consumption = .8)
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| Alveolar-Arterial (A - a) O2 Gradient | Alveolar PAO2 - Arterial PO2 = 10 - 14...the lung is not perfect
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| Causes of Hypoxemia | dec inspired PO2, hypoventilation, diffusion impairment, shunt (intrapulmonary or cardiac), V/Q mismatch
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| Low inspired PO2 | rare cause of hypoxemia, occurs at high altitude of with breathing low oxygen mixture, pts with lung disease may get more hypoxemic with exercise b/c the partial pressure change for O2 diffusion is decreased
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| Hypoventilation = Hypercapnia | always associated w/ an inc in PCO2; inc FIO2 can relieve hypoxemia; Normal A-a gradient; equals to elevated PCO2 in blood; ventilation = removal of CO2 from blood
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| Minute ventilation | respiratory rate x tidal volume; dalton's law (relationship btw PCO2 and PO2 in alveoli); defects in minute vent and tidal vol cause hypoventilation
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| Hypoventilation: causes-1 | 1. CNS/brainstem (drugs, central sleep apnea, hypothyroidism, met alkalosis, CVA); 2. Spinal cord diseases (C-3, tetanus); 3. Anterior horn cell diseases (ALS, polio, rabies); ex: morphine overdose dec vent/tidal vol; diaphragm (mechanical) affects TV too
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| Hypoventilation: causes-2 | 4. peripheral nerve disease (GBS, diptheria, fish toxins, polyneuropathy demyelination of critical illness); 5. NMJ disease (myasthenia gravis, eaton lambert, organophosphate poison, botulism); Paranchymal lung disease (COPD, endstage restrictive lung dx)
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| Diffusion properties: gases across a semi-permeable membrane | surface area, solubility, molecular weight, partial pressure difference
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| Diffusion impairment | pulm capil blood has no time to equilibrate w/alveolar gas d/t thickened blood gas barrier, esp during exercise (Idiopathic pulm fibrosis IPF , asbestosis, sarcoidosis, coll vascular dx; O2 can fix hypoxemia by inc pressure gradient; CO2 elim not affected
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| Shunt - 5% of blood in all people never sees the alveoli | *blood crossing alveoli is not oxygenated*; does NOT respond to increasing O2** a form of ventilation-perfusion mismatch where alveoli are not ventilated or participants of gas exchange (d/t edema from collapse, pus, fluid), but are still perfused
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| Types of shunts: cardiac and pulmonary | cardiac (ASD, VSD, PDA-R to L shunt); Pulmonary (paranchymal lung disease, A-V fistula from end stage liver disease); other ex: spider angiomas
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| Depression of arterial PO2 by shunting during 100% O2 breathing | the addition of a small amount of shunted blood with its low O2 concentration greatly reduces the PO2 of arterial blood; this is b/c the O2 dissociation curve is nearly flat when PO2 is very high
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| Ventilation-Perfusion Mismatch | **most common cause of hypoxemia;** there can be perfusion to areas with shuntin or w/o ventilation and ratio ~0; or there can be ventilation w/o perfusion ~infinity
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| Dead space ventilation | air isn't getting to blood (everything through terminal bronchioles before alveoli); anatomical dead space is ~a person's body weight in mL; alveolar dead space (O2 in alveoli but no blood); physiological dead space (anatomical + alveolar dead space)
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| Inequality of ventilation | breath and blood goes to lower part of the lung more than the upper part; **high V/Q ratio at top of lung and low V/Q ratio at bottom**...apex has greater ventilation than perfusion allows for TB growth
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| Hypoxemia: dec PO2 (ex: altitude) | no inc in A-a; responds to inc FiO2
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| Hypoxemia: hypoventilation | no inc in A-a; responds to FiO2
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| Hypoxemia: V/Q mismatch | inc A-a; responds to inc FiO2
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| Hypoxemia: Diffusion | inc A-a; responds to inc FiO2
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| Hypoxemia: Shunt | inc A-a; does NOT respond to inc FiO2
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| Alveolar ventilation | per inspiration is 350mL; per minute is 5250mL (tidal vol - dead space times respiratory rate = 500-150)x15)
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| Determining who will have a greater alveolar ventilation: Tidal volume of 600mL 10/min vs 300mL at 20/min | second value is rapid/shallow breathing w/150mL of dead space ventilation on each inspiration; the first person has more air reaching the alveoli for gas exchange
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| O2 Therapy: Low flow | entire minute volume is NOT supplied (some room air); variable FiO2 (O2 flow, reservoir capacity, pt's ventilatory pattern); nasal cannula, face mask, non-rebreather, trach collar
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| O2 Therapy: High flow | must supply the entire inspired gas mixture volume (3-4x pt's minute volume (ex: 500x12 = 6L; 6Lx3 = 18L dose); reservoir capacity); Ventilatory pattern doesn't affect FiO2; fixed FiO2 (maintained by meeting all inspir flow demands)
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| CO2 removal | arterial PCO2 is totally dependent and inversely proportional to alveolar ventilation; minute ventilation of 6L, but not all reaches alveoli d/t dead space ventilation
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| CO2 removal: total ventilation (VE) | VE = alveolar ventilation (VA) + dead space ventilation (VD); VA = (CO2 prod/PCO2) x K; alveolar vent determines arterial PCO2 b/c you are blowing it out; invsely prop to minute vent
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| Obstructive ventilatory defect classifications | can be reversible or not, can have diffusion impairment or not; asthmatics can't get air out d/t bronchoconstriction
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| Restrictive ventilatory defect | diffusion defect either in proportion to decreased TLC or reduced out of proportion to dec in TLC
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| Spirometry can measure: | tidal volume and vital capacity
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| Lung volume studies can measure | total lung capacity, functional residual capacity, and residual volume (need an additional measurement by helium dilution or the body plethysmograph)
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| Components of pulmonary function testing (PFTs) | 1. spirometry and flow vol loop (*effort dependent; required max effort*); 2. Lung Volumes (**effort independent** hard to mess up; closed system); 3. DLCO (**effort independent** hard to mess up; closed system)
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| Spirometry with flow volume loops | assess mechanical properties of respiratory system by measuring expiratory volumes and flow rates; requires pt to take max inspiratory and expiratory effort
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| FEV1 | forced expiratory volume 1; the vol of air/amt of vital capacity forcefully exhaled in one second
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| FVC | forced vital capacity; the vol of air that can be maximally forcefully exhaled
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| FEV1/FVC ratio | most people can blow out btw 70-80% of vital capacity in 1st second; used to measure how bad COPD is
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| FEF25 - 75 | forced expiratory flow; the average forced expiratory flow during the middle (25-75%) portion of the FVC; reduced in COPD
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| Criteria for acceptability of spirometry tests | 1. no artifact from cough, glottic closure or equip probs; 2. good start w/o hesitation; 3. good exhalation w/6sec of smooth continuous exhalation and/or a plateau in vol time curve of >1sec, or a reasonable duration of exhalation with a plateau
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| Criteria for reproducibility after obtaining three acceptable spirograms: | largest FVC and FEV1 w/in 0.2L of next largest reading; if these criteria aren't met, additional spirograms should be obtained
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| Flow volume loop | graphs pt's spirometric efforts; flow vs. volume plot shows continous loop from inspiration to expiration
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| Lung Volume Studies: Helium Dilution | measures total amount of gas in the lungs after complete inspiration; use spirometer volume and [helium equilibration] to calculate
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| Lung Volume Studies: Nitrogen Washout | pt given 100% O2 to breath for 7min after breathing room air; the maldistribution indicated by nitrogen concentration (>2.5%) is in the expired air
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| Lung Volume Studies: Body Plethysmography | similar to helium dilution test; pt sits in clear rigid chamber breathing into a valve; valve is closed and pt pants out which compresses the gas in the box; when pt pants in the opposite occurs; measure pressure changes to determine volume of pt's lung
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| Diffusion capacity | diffusion rate is proportional to: the area, partial pressure difference, solubility of gas in the tissue; Inversely proportional to: the thickness of tissue and the square root of the molecular weight; **O2 + Hb rxn rate also affects diffusion capacity**
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| Method for measuring diffusion capacity | single breath; mix CO, N2 and O2; rate of dissapearance of CO from alveolar as duing a 10sec breath hold; measure inspired and expired [CO] w/infrared; normal value is 25mL/min.mmHg; **if <25, pt has diffusion problem**
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| Factors that Decrease (DLCO) Diffusion Capacity | age, emphysema, interstitial lung disease (this is an early finding), any restrictive lung disease (-TLC), pulmonary vascular dx (+ phys dead space); anemia
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| Causes of restrictive ventilatory defect (decreased diffusion capacity) | interstitial lung dx (pneumonitis, fibrosis, edema, pneumoconiosis, granulomatosis), space occupying lesions (tumor, cyst), pleural dx (pneumo-, fibro-, hemothorax, effusion, empyema), chest-wall dx (injury, kyphoscoliosis, NM dx), extrathroacic (obesity)
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| Polycythemia | increases diffusion capacity; more Hb improves diffusion
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| Chronic cardiomyopathy | increases diffusion capacity; elevated end diastolic pressure = inc pulmonary vascular pressure which recruits more capillaries that are normally closed in upper lung field
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| Asthma exacerbation | increases diffusion capacity; inc intrathoracic pressure in asthma attack increases vascular gorging
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| pulmonary hemorrhage | increases diffusion capacity
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| Diffusion defects | w/ obstruction (emphysema); w/ restriction (all cases); w/o obstruction or restriction (early interstitial lung disease or pulmonary vascular disease)
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| Common causes of obstructive ventilatory defects | upper airway (pharynx/larynx tumor, edema, infxn; foreign body; trachea collapse, stenosis, tumors); Central and peripheral airway (bronchitis, -iectasis, -iolitis, -al asthma); Parenchymal dx (emphysema)
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| Obstructive ventilatory defects flow rates | reduced flow rates (dec FEV1, dec or nml FVC, dec FEV1/FVC); FEF 25-75 is dec; TLC is nml or inc; DLCO (diffusion capacity of carbone monoxide) is nml or dec
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| Grading of severity of obstructive ventilatory defect | FEV1: >80%, 65-80%, 50-65%, <50%
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| Bronchodilator Response | FVC: inc of 10% or more; FEV1: an inc of 200mL or 15% of baseline FEV1; FEF25-75%: inc of 20% or more
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| Sin quanon for asthma (hyperreactive airway disease) | **reversible obstructive ventilator defect*
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| Non-reversible fixed obstructive ventilatory defects | chronic bronchitis, emphysema
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| Sin quanon for restrictive ventilatory defect | **<80% of predicted TLC for age, height, weight, ethnicity; low DLCO too
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| Restrictive lung disorders | (blank)
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| Obstructive COPD | the opposite of restrictive ventilatory disease
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| FVC of 78%, FEV1 of 72%, FEV1/FVC of 94% | the reductions preserve the ratio and this pt therefore has a RESTRICTIVE lung disease
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| FVC of 119%, FEV1 of 111%, FEV1/FVC of 94% | this pt is normal; all values are 80 to 120% of predicted values
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| FVC of 77%, FEV1 of 87%, FEV1/FVC of 115% | pt is restricted?? w/o seeing TLC
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| FVC of 94%, FEV1 of 47%, FEV1/FVC of 50% | pt is obstructed...they can only blow out 39%!!
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| Interpreting Spirograms: early obstruction | FEV1/FVC is <80% OR FEF25-50% <50%
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| Interpreting Spirograms: Obstruction | FEV1 <80% and FEV1/FVC <80% or <2 SD below predicted age
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| Interpreting Spirograms: Possible Restriction | FEV1 <80% and FEV1/FVC >80%; get lung volumes to confirm
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| Interpreting Spirograms: Pure Obstruction | FEV1 <80% and FEV1/FVC <80% or <2 SD below predicted age; FVC >80%; grade based on decrement in FEV1
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| COPD - general | grp of Dxs w/obstructive ventilatory defect usu a/w smokin; 15 mill Americans (12-chronic bronchitis, 3-emphysema); 5th leading cause of death; 10yr mortality >50%; not much research when compared to asthma
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| Risk factors for COPD | smoking (80-90%); 2nd hand smoke, air pollution, hyperresponsive airways; M>F, whites, alpha-1-antitrypsin deficiency (<1%)
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| Clinical Features of COPD | 20 pack years; usu 40s; cough, mucous, SOB, wheezing, barrel chest (hyperinflation), prominent accessory mm; low/flat diaphragm, diminished breath sounds
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| New COPD Definition | preventable, treatable dx state w/partially reversible airflow limitation that is progressive & a/w abnml inflam response to noxious particles like smoke; systemic consequences too
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| COPD Pathogenesis | tobacco smoke causes chronic inflam (CD8 Tcells, MQs, PMNs, IL-8, TNFa); oxidative stress & proteinases cause damage (host protective factors aren't sufficient; leading to chronic bronchitis or emphysema
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| Obstructive Ventilatory Diseases: Asthma versus (COPD) | sensitizing agent (noxious agent); inflam d/t CD4+, eosinophils (CD8+, PMNs, MQs); airflow limitation completely reversible (~completely irreversible)
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| more COPD pathophysiology | inc mucous/dec mucociliary clearance (cough/sputum); loss of elastic recoil (airway collapse); inc smooth muscle tone; pulmonary hyperinflation; abnml gas exchange (hypoxemia and/or hypercapnia)
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| Early COPD Damage: Peripheral Airways (*major site of expiratory obstruction*) | diameter <2mm; inflam; repeated cycles of injury/repair; tissue remodeling and scarrin; lumen narrowing and fixed obstruction; inflam = edema, mucous hypersecretion obstruction
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| COPD: expiratory airflow limitation | irreversible, mainly d/t remodeling of small airways that then inc resistance
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| COPD Damage: Lung parenchyma | dilation/destruction of bronchioles & alveoli in upper lobes (**except alpha-1-antitrypsin def is in lower lobes**); d/t imbalance of proteinases and antiproteinases; inc airway resistance (loss of elastic recoil/alveolar attachments to peripheral airway)
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| COPD Damage: Pulmonary Vasculature | smoke causes endothelial dysfxn, thickening of intima, inc smooth muscle cells and tone; chronic hypoxemia causes further vasoconstriction; can lead to pulmonary HTN and cor pulmonale
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| COPD: Gas exchange problems | **hypoxemia d/t V/Q mismatch** usu occurs when FEV1 <1L; loss of surface area (destruction of alveoli and capillaries) can reduce diffusion capacity
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| Low O2 in emphysema | peripheral airway narrowing from dec recoil; destruction of alveoli and alveolar capillary
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| Low O2 in chronic bronchitis | aiway narrowing from inflammation, dec ventilation and alveolar PAO2; remodeling and scarring d/t injury
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| Components of respiration | 1. bellows: functional pump (dependent on thoracic-abdominal structures and diaphragm); 2. lungs: function-gas exchange (dependent on airways, parenchyma, capillaries)
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| Pathological Changes with Emphysema: dec lung elastic recoil pressure | dec max expiratory flow rate; dec driving pressure; destabilized intraparenchymal airways; elastic recoil of lung aids in expiration in returning to FRC; at FRC outwards spring of chest aids in inspiration...FRC (fxnl residual capacity) is like tug of war
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| Pathological Changes with Emphysema: Inspiration and Expiration | 1. hyperinflation inc resting vol above FRC; more effort required to distend thorax during inspiration; 2. diminished elastic recoil pressure inc need for respiratory muscle activity
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| Experimenting with your own FRC: | take a breath, don't exhale and breathe on top of that - it is above FRC; there is reduced elastic recoil
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| Pathological Changes with Empysema: Hyperinflation and effect on diaphragm | shorten muscle fibers (less force); dec diaphragmatic curvature (less trans-diaphragmatic pressure; La Place's law); medial orientation of diaphragmatic fibers (Hoover sign); Dec zone of opposition
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| Hyperinflation and Effect on Chest Wall | enlarged retrosternal space (btw mediastinum and ant chest wall); horizontal ribs (normally oblique); thoracic cage elastic recoil directed inwards (inc elastic load) normally outwards
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| Overall Effects of Hyperinflation | inc work of breathing, dec inspiratory capacity, dec inspiratory force by diaphragm, inefficient diaphragm; it takes longer to exhale w/much less efficiency
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| Chronic Bronchitis and Emphysema defined (usu pts have a combo of both) | chronic productive cough for 3 months in each of 2 successive years; pathologically characterized by submucosal hypertrophy and inflammation; characterized by destruction of acinus or secondary lung lobule distal to the terminal bronchial
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| Emphysema and (bronchitis) | Onset: 60yo (50); Dyspnea: severe (mild); Sputum: scant (copious); CXR: hyperinflated (inc markings of thickened airways); PAO2: 65-70 (45-65); PACO2: 35-45 (50-60); HCT: 35-45 (50-55); Cor Pulm: rare (common); Pink Puffer (blue bloater)
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| Increased markings in chronic bronchitis CXR | indicative of thickened airways; these pts retain more CO2 than emphysema; they develop polycythema and peripheral edema d/t cor pulmonale, RHF and back up of fluid;
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| PCO2 sin quonon | alveolar ventilation; if alveolar ventilation is decreased, minute ventilation is dec and you aren't breathing that hard
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| FEV1 Decline: natural aging | after age 25-30 FEV1 declines 30mL per yr; 85-90% of heavy smokers have greater decline; 10-15% of heavy smokers w/alpha-1-antitrypsin def decline 150mL/yr; *if smoker quits lung fxn not regained, but rate of decline returns non-smoker rate*
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| Goal of COPD Therapy | *Prolong Life (stop smoking, administer O2); minimize progression of air flow obstruction (delay rate of FEV1 decline); ID alpha-1-antitrypsin def pts w/screening
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| Management of COPD: Stage 0 "at risk" | risk factors, chronic cough/sputum, spirometry not abnml; Tx: adjust risk factors, immunize
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| Management of COPD: Stage 1 "mild COPD" | FEV1/FVC <70%, FEV1 >80%, w/ or w/o symptoms; Tx: short-acting bronchodilator as needed
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| Management of COPD: Stage 2 "moderate COPD" | FEV1/FVC <70%, FEV1 btw 50-80%; w/ or w/o symptoms; Tx: one or more long-acting bronchodilators and rehabilitation
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| Management of COPD: Stage 3 "severe COPD" | FEV1/FVC <70%, FEV1 btw 30-50%; w/ or w/o symptoms; Tx: one or more long-acting bronchodilators, rehab, inhaled glucocorticosteroids if repeated exacerbations >3yrs
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| Management of COPD: Stage 4 "very severe" | FEV1/FVC <70%, FEV1 <30%, respiratory or RHF; Tx: 1 or more long-acting bronchodilators, inhaled glucoCCteroids (if >3yrs); Tx complications, rehab, long-term O2 therapy for respiratory failure, surgery?
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| Management for all COPDers | get flu vaccine yearly, pneumococcal vaccine once; STOP smoking (tx psychological and physical/chemical addiction separately)
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| Pharmacotherpay for Stable COPD: Bronchodilators | short acting b2 agonist (salbutamol); long acting b2 agonist (salmetrerol and formoterol); Anticholinergics (Ipratropium, Tiiotropium); Methylxanthines (theophylline)
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| Pharmacotherpay for Stable COPD: Steroids | Oral (prednisolone); Inhaled (fluticasone, budesonide)
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| Why Bronchodilators? | may inc airflow and dec dyspnea; b2 agonists aren't ideal (Ipratropium (up to 6puff 4x/day) is better and works synergistically); d/t slow onset of action shouldn't be a PRN drug;
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| How do bronchodilators work? | reverse inc bronchomotor tone; relax smooth muscle, reduce hyperinflation, improve breathlessness
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| When do you start an anticholinergic (the COPD #1 med) to act at the muscarinic receptors and block ACh-induced bronchoconstriction? | when pt has daily symptoms, regular use of ipratropium is recommended; more effective & less side effects than b2 agonists; dec mucous hypersecretion; **cholinergic tone: the only reversible component of COPD (nml airway has small degree of vagal tone)**
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| Tiotropium in COPD | specific M1 and M3 muscarinic blocker; inc FEV1 and FVC, no tachyphylaxis, dec use of rescue albuterol, dec wheezing/SOB, caused dry mouth in few
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| Theopylline in COPD | very dangerous and worthless; pt can die d/t seizures and cardiac arrhythmias; should NOT be given to COPD
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| Corticosteroids in COPD | never really a reason to use for COPD; oral can cause glaucoma, cataracts, osteoporosis, AVN, diabetes; inhaled have limited benefit; FEV1 may improve
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| Oxygen therapy in COPD | increases lifespan in hypoxemic COPD; inc exercise tolerance; (Caution: ptw w/PO2 >60, but DLCO <65% will desaturate w/exercise)
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| Pulmonary Rehab in COPD | education, psychosocial counseling; stop smoking, O2 Rx, exercise, nutrition (malnutrition in 25% outpt and 50% inpt); PT/OT; breathing exercises; Look into inc exercise tolerance COPDers may just be out of shape...limit disability to dx not their fitness
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| Bullectomy in COPD | indicated in pts w/large bullae and compressed good lung tissue; there is a high surgical morbidity; bullae usu in upper lobes; if you remove it the diaphragm can gain back some mechanical capabilities
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| Lung Transplant in COPD | single or double lung; indicated for endstage emphysema (refractory to med Tx); disabling dyspnia, FEV1 <35% of nml; hyperinflated lungs; bullous or diffuse emphysema
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| Lung Transplant in COPD: Contraindications | tobacco use w/in 3-6mo b/f surgery; obesity or cachexia, unstable coronary dx or other med condition, prior thoracotomy or pleurodesis on side of surgery; pulm HTN, can't rehabilitate, terminal dx, severe hypercapnia (>60mmHg)
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| Surgical Options with the Lung | Giant bullous disease (bullectomy); Lung Vol Reduction Surgery (FEV1 <20%, diffuse/upper lobe emphysema); Lung Transplant (FEV1 <25%, young pt, 3-5yr mortality is 55%)
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| Differential Diagnosis of Exacerbation of COPD | infxn (bronchitis - bacterial or non); pneumonia, pulmonary embolus, pneumothorax, CHF, arrhythmias, chest wall/pleural abnormality)
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| COPD and CHF: cor pulmonale, left sided heart failure: therapy | O2, diuretics, nitrates (coronary artery disease)
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|
||||
| COPD and Arrhythmias: Tx | supraventricular (multifocal A-tach, supra V-tach, A-fib, A-flutter); Ventricular arrhythmias, electrical mechanical dissociation; Treat hypoxemia, acidosis, electrolytes, drug toxicity, CAD, 1* arrhythmia disorder)
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|
||||
| COPD and Pulmonary Embolism | inc risk of association; high index of suspicion
🗑
|
||||
| COPD and Chest Wall or Pleural Abnormality | pleural effusion, rib fx or chest wall trauma, pneumothroax, upper airway obstruction
🗑
|
||||
| Considering antibiotics for COPDers | usu trachea is sterile, but 80% of people w/chronic bronchitis have bacteria colonizations; you must treat if: sputum is green/purulent, sputum vol inc or inc dyspnea; you can give amoxicillin to shut pt up b/c most infxns are resistant to it!!
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|
||||
| Bacterial pathogens in COPD | 50% of infections; H. influenzae (some amox and cefaclor resistance); S, pneumoniae (some TCN resistance); M. catarrhalis (amox resistant)
🗑
|
||||
| Non-bacterial pathogens in COPD | 50% of infxns; viruses (RSV, influenza, parainfluenza, rhinovirus, coronavirus); mycoplasma pneumoniae, chlamydia pneumonia...
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|
||||
| Treating exacerbations of COPD | 1. correct hypoxemia w/O2 therapy; 2. correct acidosis (intubate, bicarb tx; aggressive); 3. underlying dx (tx airflow obstruction b-adenergics/anticholinergics w/respiratory therapy to bring up secretions) and address precipitating event
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|
||||
| Cystic Fibrosis: stats | auto recessive; median age of survival is improving ~32; death usu cardiorespiratory; manifests in sinuses/lungs, GI tract, nutritional status; Vicious cycle of obstruction, inflammation and infection
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|
||||
| Cystic fibrosis: sinus/pulmonary manifestations | sinusitis, **nasal polyps;** bronchitis/pneumonia (tx acute viral infxns to prevent colonization), bronchiectasis, asthma (inc incidence b/c of chronic inflam), allergic bronchopulmonary asperigillosis (inflam rxn, high IgE 100x nml; allergic damage)
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|
||||
| Cystic fibrosis: Gastrointestinal tract manifestations | **meconium ileus and rectal prolapse (chronic constipation);** distal intestinal obstruction (impacted stool in jejunum); biliary cirrhosis (not common), portal HTN, obstructive jaundice/gallstones; palpable spleens; pancreatitis (destruction of islets)
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|
||||
| Cystic Fibrosis: Nutritional Manifestations | malabsorption; steatorrhea; FTT; protein deficiency; fat soluble vitamin deficiency; *pancreatic enzymes can't dump b/c ducts are plugged and pt cannot absorb fats and vit A, D, K* stools float and stink bad; can't gain weight
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|
||||
| Cystic Fibrosis: other manifestations | delayed puberty (self conscious for being short), impaired fertility (usu male, but females may have difficulty delivering), diabetes mellitus, hyponatremia (sweat), coagulation defects (d/t def in vit K), anemia, digital clubbing (from chronic hypoxemia)
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|
||||
| Cystic Fibrosis: Evaluation | **sweat chloride, if >60 it's positive** DNA (delta F508 mutation in caucasians); spirometry (lung vol); CXR (bronchiectasis), sinus Xray; blood gas, sputum cultures
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|
||||
| CF: Bronchiectasis | dilated 1-1.5x accompanying blood vessel; loss of normal tapering of airway towards periphery; thickened airway walls; varicose constrictions of airway; ballooned cysts at ends of bronchus
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|
||||
| Symptoms of Bronchiectasis | chronic cough, mucopurulent secretions; dyspnea; hemoptysis; fever; fatigue; pleuritic chest pain; wt loss
🗑
|
||||
| Pathophysiology of bronchiectasis | genetic predisposition; altered bronchial dynamics, ineffective mucus clearance, chronic or recurrent infxn, bronchial wall inflam & destruction; it keeps going...; can be cylindrical (mc), varicose (focal constrictions) or saccular (cystic-most severe)
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|
||||
| Airway pathogens by age | staph is being replaced by pseudomonas in older age groups (10yo+); it produces a slime on top of the mucous, so it is almost impossible to irradicate; leads to chronic infxn and is more pathogenic than staph (faster decline/death)
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|
||||
| Goals of CF therapy | improve life; inc lung fxn, dec resp symptoms, dec irreversible lung damage; dec infectious exacerbations,dec use of parenteral antibx, dec days missed in life; 2yr survival rate drops 50% in their 20s when lung fxn starts declining
🗑
|
||||
| Cystic Fibrosis Therapies | bronchodilator, chest physiotherapy, oral/IV antibx, nebulized antibx, mucolytics (ex: inhaled DNAse), anti-inflam, enzyme (pancreatic)/vitamin supplements to improve nutrition w/meals
🗑
|
||||
| Airway hygiene techniques | chest percussion and postural drainage, autogenic drainage, positive expiratory pressure (PEP), flutter valve (like a kazoo sends pressure/vibrations to mobilize secretions), intrapulm percussive ventilation, high freq chest compression (chest vest)
🗑
|
||||
| Antibiotic selection for CF | size matters (avoid inc airway deposition from hi dose and alveolar absorption/systemic toxicity if too low); inhaled antibx get to sputum not serum;
🗑
|
||||
| Inhaled Tramycin | indicated for CF; uses nebulizer; inc FEV1 significantly over 24wks; killed off pseudomonas; helped gain weight; dec hospitalization and absenteeism; BUT it may cause ototoxicity
🗑
|
||||
| Pulmozyme | indicated for CF; nebulized antibx; daily admin maintains efficacy; dec rate of RTI requiring parenteral antibx; improves pulm fxn and pt well-being;
🗑
|
||||
| Occupational lung disorders | pneumoconiosis, inhalation injury/irritant exposure; occupational bronchitis, occupational asthma, hypersensitivity pneumonitis
🗑
|
||||
| Pneumoconiosis | *usu Silica, Asbestos, Coal;* may take 20yrs to present; depends on intensity/duration of exposure to agent; non-malignant condition d/t inhalation of organic minerals and dusts that cause a rxn in the lung tissue
🗑
|
||||
| Pneumoconiosis pathophysiology | particle in lung, MQ engulf/transports to mucus/lymph; system overloads & particles accumulate in alveoli; triggers inflam immune response; fibroblasts secrete reticulin, entraps MQs; results in interstitial fibrosis (clog arterioles..ischemic necrosis)
🗑
|
||||
| Pulmonary Massive Fibrosis (PMF) | endpoint of pneumoconiosis (radiographic changes in superior segments of upper lobes)
🗑
|
||||
| Coal macules | halmark of coal worker's pneumoconiosis; extend forming emphysema
🗑
|
||||
| Silicosis | mc pneumoconiosis in world; d/t mining, blasting, drilling, etching, ceramics; Causes intense fibrotic rxn (simple silicosis or more severe form: Progressive Massive Fibrosis); **inc rate of lung CANCER and propensity for infxn;** restrictive/obstructive
🗑
|
||||
| Asbestosis | **a/w shipyard, pipefitters, plumbers, insulation workers;** **Fibrotic rxn leads to progressive restrictive lung infxn and CANCER** there is a 6-FOLD INC for cancer (MESOTHELIOMA)/COPD when pt smokes!!; presents like bronchitis (SOB, cough, inc sputum)
🗑
|
||||
| Coal Workers Pneumoconiosis (CWP) | "black lung;" no signs, initially asymptomatic; chronic cough/sputum; PMF; **Coal Macule Lesion - pin-sized grp of MQs filled w/black coal in superior lobe;** inc risk for EMPHYSEMA, smoking inc morbidity; a/w RF levels...don't inhale coal dust!
🗑
|
||||
| Caplan Syndrome* | PMF a/w rheumatoid arthritis; lesions located on **peripheral lung fields;** nodules progress faster than PMF and may precede RA
🗑
|
||||
| How to determine Pneumoconiosis? | take a detailed history (esp of job description, smoking hx, any possible exposures, time, etc)
🗑
|
||||
| Pneumoconiosis diagnostics | CBC, sputum culture, CXR/CT, PFTs, BAL (bronchoalveolar lavage); bronchoscopy
🗑
|
||||
| Pneumoconiosis treatment | Tx symptoms; O2, bronchodilators, immunizations for flu/pneumococci; serial CXR, look for signs of cancer, minimize exposure, transfer jobs
🗑
|
||||
| Dx of mesothelioma | CXR L-lung pleural thickening w/infiltrate; neg cardiac enzymes, WBC 16,000; positive D-dimer; PE on CTscan near mediastinum; pt admitted, heparin IV, Abx; lung biopsy...she used to shake out husband's clothes (he was a plumber...asbestosis)
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|
||||
| States w/high prevalence of coal miner's lungs: | eastern PA, western MD, WV, VA, KY; 30% can develop CWP, 16% pulmonary fibrosis, 2.5% PMF; Great Britain has 16% PF; no predilection for sex, race, age
🗑
|
||||
| Asthma | chonic inflam dx of hyper-responsive airways (mast cells, eosinophils, Tlymphocytes); SOB, cough, wheezing; widespread/variable airflow limitation that is reversible w/ or w/o treatment; **obstructive ventilatory defect; Hypoxemia d/t a V/Q mismatch**
🗑
|
||||
| Types of Asthma | 1. Extrinsic (atopic; d/t genetic sensitivity usu to aeroallergens; IgE-antigen triggers acute allergic response; usu childhood-YAhood); 2. Intrinsic (nonatopic; older, late onset of asthma)
🗑
|
||||
| other types of asthma | exercise-induced, nocturnal, aspirin-induced, occupational, cough-variant, ABPA, fatal/near fatal asthma
🗑
|
||||
| Components of airway obstruction | bronchospasm, mucus accumulation w/plugging; inflammation w/edema
🗑
|
||||
| Pathology of advanced chronic asthma | Significantly Reversible (hyperinflation, thick mucus/mucus plugs, peribronchial eosinophilic infiltrate); inc # of mucous glands, muscular hypertrophy, thickened basement membrane
🗑
|
||||
| What makes asthma worse? | animal dander (warm-blooded pets); house dust mites, roaches, pollens from grass/trees; molds (indoor and outdoor); irritants (non-organics), URT infxns, exercise, crying/laughing, changes in temp/weather
🗑
|
||||
| Asthma targets and mechanisms | 1. acute inflam (bronchoconstriction, edema, secretions, cough); 2. Chronic inflam (cell recruitment, epithelial damage, early structural changes); 3. Airway remodeling (cellular prolif, ECM increase)
🗑
|
||||
| Cromones, Asthma - mechanism of action | inhibits mast cell degran; inhibits IL-4-induced IgE synth; inhibits activ of inflam cells; acts as local anesthetic; promotes relaxation by altering (dec?) Ca influx into cell
🗑
|
||||
| Beta agonists and xanthines, asthma - mechanism of action | used most often; dec chemical mediator release causing dilation via dec Ca; Ca is reduced when cAMP is elevated by adenylate cyclase; Theophylline is less common (blocks phosphodiesterase from inhibits cAMP, resulting in elevated cAMP and dec Ca)
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|
||||
| Antileukotriene drugs and asthma: receptor antagonists | Zafirlukast (accolate), pranlukast (ultair), montelukast (singulair), cinalukast
🗑
|
||||
| Antileukotriene drugs and asthma: leukotriene synthesis inhibitors | Zileuton (zyflo), Bay x1005, MK-886, ZD 2138, RG 12535
🗑
|
||||
| Glucocorticoids (GCS) | the primary anti-inflammatory therapy for asthma and related disorders; Transrepression (neg modulation of gene transcription); **Transactivation (induction of gene transcription) - this is more optimal
🗑
|
||||
| Budesonide | a GCS that greatly dec the number of eosinophils in the airway
🗑
|
||||
| So, if most anti-asthma therapies target symptoms and inflammtion, why is there a decline in lung function over time? What is effect on airway remodeling? | difficult to pinpoint; poorly understood area; sub-epithelial fibrosis and coll III levels (inc fibroblasts, mast cells, Tcells) may inc when therapy is stopped; **GCS have little or no effect on airway remodeling (may inc prolif of smooth m/fibroblasts**
🗑
|
||||
| Limitations of asthma medications | no cure, little evidence in prevention, pts still at risk for symptoms/exacerbations, mortality still a severe problem; meds have adverse effects
🗑
|
||||
| Where to target novel asthma therapies? | antigen, Th2-cell stimulation and release of Th-2 cytokines, mast cell activation (IgE), eosinophil recruitment/activation, upregulation of adhesion molec expression in vessels/epithelium, activate resident cells (ex: fibroblasts)
🗑
|
||||
| Asthma, can we target the inflammatory cascade? What's included? | need to develop inhibitors, antagonists or antibodies to: IL-9, IL-5, IgE, IL-4/IL-13, NFkB (transcription factor)
🗑
|
||||
| Anti-IgE: Omalizumab | humanized monoclonal Ab; SQ injection; binds IgE; can reduce asthma exacerbations and dec use of ICS in pts w/allergic asthma; very expensive, risk of anaphylaxis, possibly carcinogenic
🗑
|
||||
| IL-5 monoclonal antibody | sustained and potent inhibition of circulating eosinophils (allows biannual injections); BUT no effect on early or late phase allergen response and no effect on methacholine challenge...questions the importance of eosinophils to asthma
🗑
|
||||
| b2 adrenergic bronchodilators and asthma | inhaled (Salbutamol/Ventolin, feoterol/berpotec, procaterol/Pro-Air) quick relief; take as needed; some are slow-acting; possible tremor/palpitation
🗑
|
||||
| Theophyllin bronchodilators and asthma | *poor bronchodilator; can be used in Asthma b/c smooth muscle is inflamed, but NOT FOR COPD which is a fixed disease** uniphyl, theodur; pill form, used less often
🗑
|
||||
| Anticholinergic bronchodilator | NOT for ASTHMA, **Use for EMPHYSEMA** ipratropium bromide (atrovent); used in conjunction with b2 adrenergic agent (ventolin)
🗑
|
||||
| NSAIDS and asthma | cromoglycate/chromolyn; intal; preventative for mild asthma in children; inhaled nedocrimil sodium (tilade), oral ketotifen (zaditen)
🗑
|
||||
| Steroidal compounds: inhaled | **most efficacious for use in ASTHMA, NOT COPD** beclovent, budesonide; inc FEV1, reduces and prevents inflamm; improves sleep/exercise performance; side effects (wt gain, burning sensation - rare/mild)
🗑
|
||||
| Steroidal compounds: oral | prednisone; for poorly managed asthma and emergency situations; safer than once thought
🗑
|
||||
| Mild intermittant asthma | symptoms <2x/wk, at night <2x/mo; FEV1 >80%; use bronchodilator therapy, short-acting b2 agonist PRN (never around the clock); *if the pt needs it all day, they have persistant asthma
🗑
|
||||
| Mild Persistant Asthma | symptoms >2x/wk 1 at night 2x/mo; FEV1 >80%; **use anti-inflamm Rx (inhaled steroids or leukotriene modifier);* also prescribe a short-acting b2 agonist as needed for bronchodilation
🗑
|
||||
| Moderate Persistant Asthma | daily symptoms w/daily rescue b2 use; >2exacerbations/wk & 1 at night/mo; FEV1 btw 60-80%; use bronchodilator therapy (long-acting b2 agonist or add theophylline; short acting b2 agonist PRN) and/or inc their anti-inflam therapy
🗑
|
||||
| Severe persistent asthma | continuous symptoms, limited physical activity, frequent exacerbations, frequent nighttime symptoms; FEV1<60%;use anti-inflam rx (inhaled steroids and maybe pulse oral steroids for 4-5days); Bronchodilator therapy (long acting b2 agonist and theophylline)
🗑
|
||||
| Risk factors for life threatening asthma (LTA) | severity of dx (previous intubation; stasus asthmaticus, hypercapnea); >55yo; African American (younger death rate 3x higher); poor, urban, psychiatric condition, noncompliance, delay in outpt steroid therapy
🗑
|
||||
| Life threatening findings | level of consciousness, **inability to speak**, dec/absent breath sounds, central cyanosis; (ominous = accessory mm; pulsus paradoxus; diaphoresis) (less severe: dyspnea, wheezing)
🗑
|
||||
| Objective criteria of severe asthma | peak flow measurements (b/f and after bronchodilator tx...not if LTA); arterial blood gas (if FEV1<1L/min or peak flow <150L/min)
🗑
|
||||
| Classical stages of Arterial Blood Gases (ABGs) in asthma | Stages 1/2: pt hypervent; Stage 3/4: pt is tired pCO returns nml w/fatigue as pO2 drops; pH inc, pCO2 dec (sin quonon of pCO2 is alveolar vent.); double alveolar vent = pCO2 halved (inverse proportion; low pCO2 is hypervent); pO2 is low d/t V/Q mismatch;
🗑
|
||||
| Endotracheal Intubation | only 8% of asthma cases need this procedure (cardiac arrest, respiratory arrest, impending respiratory arrest - altered mental state, severe tachycardia/tachypnea, diaphoresis); mild-moderate respiratory acidosis often can be reversed
🗑
|
||||
| Post-intubation | procedure-induced bronchospasm can be treated w/atropine; hypotension common (tx w/fluid bolus)
🗑
|
||||
| Allergic Asthma: control factors contributing to hypersensitivity | allergens, occupational exposures, irritants; contribution of other factors (colds/sinuses, GERD, drugs (aspirin, non-selective b-blockers), viral URI, sulfite sensitivity in food/drinks)
🗑
|
||||
| How to reduce exacerbations of Allergic Asthma? | reduce exposure; dust mites, pets, roaches, molds (air conditioner, close windows, clean, dec inside humidity, etc; Allergen Immunotherapy if exposure is unavoidable; document work exposure and plan avoidance; smoke avoidance; vaccinate
🗑
|
||||
| Single drug therapy for M. tuberculosis | contraindicated d/t rapid development of resistance; Directly Observed Therapy is recommended
🗑
|
||||
| Three stages of M. tuberculosis | TB exposure (exposure/inhalation of viable TB bacterium); TB infxn (the inhaled/ingested bacteria multiply & develop into an infxn but are sequestered by cellular immune system; no disease); TB disease (infxn progresses to disease now or after 20-40yrs)
🗑
|
||||
| Diseases caused by M. tuberculosis | pulmonary TB, extrapulmonary TB (meningitis, lymphadenitis, genitourinary TB, gastrointestinal TB, disseminated (miliary) TB; TB in HIV-infected pts (brain, pericardial, disseminated)
🗑
|
||||
| TB epidemiology | 3rd cause of death worldwide (behind malaria & diarrhea); 1/3 of world's pop infected (2mill deaths/yr); co-infxn w/HIV has inc recent incidence of TB; also immigrants (Africa, SE Asia, India), homeless, IVDA, inner city, institutions (psych/prisons)
🗑
|
||||
| Cardinal symptoms of Pulmonary TB | fatigue, wt loss, fever, night sweats; if pt is <30 and in a high risk group, consider TB; PPD+, AFB in sputum is diagnostic; (other symptoms: kids usu asymptomatic, hemoptysis a/w later cavitary stages; no chest pain/dyspnea; routine labs nml!)
🗑
|
||||
| Location of primary versus reactivation/secondary pulmonary TB | infiltrate in one or more lobes vs. apical pulmonary infilatrates
🗑
|
||||
| Pulmonary TB pathology | granuloma formation, scarring, calcifications, old collapsed cavities or fibrosis; may masquerade as malignancy, embolism or other pneumonias; DDx includes other mycobacterial infxn, fungus or virus
🗑
|
||||
| Extrapulmonary TB | only 20% of cases (80% pulm); mc in immunocompromised incl infants/children; mc sites are meninges and lymphatics; miliary TB (a/w HIV) disseminates thru blood to many organs; symptoms depend on organ involvement
🗑
|
||||
| PPD test | purified ptn derivative (mantoux test); TB cell wall injected intradermally on volar surface of forearm; MUST read w/in 48-72hrs for INDURATION (not redness)
🗑
|
||||
| Positive PPD results: 5mm induration | person in high risk group for infxn (ex: HIV pts, close contacts of active TB pts, pts w/abnml CXR)
🗑
|
||||
| Positive PPD results: 10mm induration | in persons from areas where incidence of TB is significant (SE Asia, Africa, India, Pacific Islands, Central/South America, IVDA, long-term facilities, underserved/poor populations; person is otherwise healthy
🗑
|
||||
| Positive PPD results: 15mm induration | considered the positive cut-pt for populations w/low incidence of TB, such as rural America; minimizes the possibility of false-positive rxns from cross-rxn w/other myocbacteria
🗑
|
||||
| PPD caveats | pts w/impaired cellular immunity (ex: HIV) may have negative PPD results they should have other skin tests planted when doing a PPD to indicate whether any rxn is possible; older pts w/ past infxn may need a second PPD test a week later correct result
🗑
|
||||
| The gold standard for TB diagnosis is: | culture (look for AFB red snappers) and sensitivity testing; start treatment before results (can take up to 6wks) and start heavy to avoid a resistance pattern
🗑
|
||||
| Considerations for choosing a TB treatment regimen | probability of primary resistance, previous Rx for TB, liklihood of compliance, other coexisting illnesses, specific strain sensitivities, allergies, drug rxns, hypersensitivies, immigration hx, miami/NYC
🗑
|
||||
| Choices for first line TB therapy | Ethambuto (ETB), Isoniazid (INH), Pyrazinamide (PZA), Rifampin (RIF), Streptomycin (SM); usu begin with SM plus 3 others
🗑
|
||||
| Choices for 2nd line TB therapy | amikacin (AK), capreomycin (CAP), ciprofloxacin, clofazimine (CLO), cycloserine (cyclo), ethionamide (ETH), para-amino salisylic acid (PAS), rifabutin, ofloxacin
🗑
|
||||
| TB therapy guidelines | Tx is the same for pulmonary and non-pulmonary TB; continues for >4mo; 6mo-1yr for HIV or non-compliant pts or those with resistance; do sputum cultures at 2mo and 6mo
🗑
|
||||
| Major side effects of TB therapy | **Streptomycin - OTOTOXIC;** ethambutol - optic neuritis, isoniazid - hepatitis, periphreal neuropathy, rifampin - elevated LFTs, flu-like symptoms...you must weight the toxicities w/pt
🗑
|
||||
| Preventive Treatment | individuals w/positive PPD, neg CXR and neg sputum should be treated preventively w/ INH, 300mg PO for 6mo; close household contacts of individuals w/active pulm TB should get INH regardless; multiple PPD tests can cause ulcers if + more than once
🗑
|
||||
| Preventive treatment for health care workers | recommended to have regular PPD tests yearly; previously positive health care workers should be treated preventively or for the active disease, but should have no further PPD testing; suspected TB pts should be in isolation to avoid aerosol/droplet spread
🗑
|
||||
| Aerosol spread of TB | closed spaces (modern buildings, planes and submarines w/continuous recirculating air supply are prime areas for TB spread; UV lights in ventilation systems help sterilize the air
🗑
|
||||
| Exceptions to INH therapy | people over 35, pre-existing liver disease, pregnant women; only take in restricted circumstances d/t risk of drug-induced hepatitis (which may kill pts b/f the TB does)
🗑
|
||||
| Why is TB on the rise? | *HIV/AIDS (this combo presents the greatest health risk to the general public and the health care profession)*; the TB control intrastructure was dismantled; there is an increase in immigration from countries with high prevalence of TB
🗑
|
||||
| Why are AIDS patients susceptible to TB? | *cell mediated immunity is critical in preventing "TB infection" from progressing to "TB disease"* MQs (ingest/transport bacilli) & CD4 cells (produce INF); when CD4 cells are depleted, MQs phagocytyze bacilli CD8 cells aren't recruited to kill
🗑
|
||||
| Relative risk for HIV pts to develop TB | In non-HIV pts, 80% have pulm TB; In HIV, 2/3 have both pulm & disseminated; HIV pts have 100 greater risk for TB than non-TB (other immunosupp = 10x)
🗑
|
||||
| Prevalence of HIV-TB infection | East Africa: 70-80%, US: 5%; yet, TB accounts for 25-35% of all deaths in both groups; both diseases must be treated to prevent progression; 70% of new TB cases are in HIV pts in: NY, Miami, hispanics, Afr. Amer
🗑
|
||||
| TB can appear at any stage of HIV infection | Partial loss of CD4 (mostly pulm w/upper lob infiltrates & cavitation); AIDS by CD4 count/viral load (miliary infiltrates, intrathoracid lymphadenopathy, NO cavities); Advanced AIDS (disseminated disease, lymphatic, pleural & pericardial infxn, meningitis
🗑
|
||||
| Presentation of TB in HIV pts | in pts w/nml immunity, the primary TB lesion heals and calcifies and is visible as Ghon body on CXR; HIV-infected pt may have full blown TB as their "AIDS-difining illness"
🗑
|
||||
| Other TB diagnostic modalities | Nucleic acid amplification (rapid, low sensitivity, $$$); Cytokine release assay (rapid, sensitive, specific, but can't tell if infxn is active); BAL (invasive, effective, $$$), lymph node, liver, marrow biopsies, CSF
🗑
|
||||
| Tx for TB in HIV pts | pts taking PIs or nnRTIs should NOT take Rifabutin; those taking Ritonavir shoudn't get Rifampin or Rifabutin; Prophylaxis: INH, pyridoxine (if INH-resistant): 9mo; Rifabutin or Rifampin: 4mo; MDR-TB check w/dept of health
🗑
|
||||
| M. avium/intracellulare | causes serious pulmonary and disseminated disease; may also cause bone and joint infxn, lymphadenitis (in kids), fasciitis or deep tissue infxn
🗑
|
||||
| M. avium/intracellulare diagnosis | CXR, sputum AFB stain, sputum culture and sensitivities **must differentiate from M. tb b/c therapy is different;** culture of other affected areas
🗑
|
||||
| M. avium/intracellulare therapy | Clarithromycin (macrolide) + Ethambutol + Rifabutin for 12-24mo (possibly for life)
🗑
|
||||
| M. avium/intracellulare prophylaxis | Azithromycin, Clarithromycin, Ethambutol, Rifabutin; may discontinue if CD4 count goes above 100/mL for six months, otherwise stay on it for life
🗑
|
||||
| M. kansasii | causes pulmonary infxn resembling M.tb; usu seen in tertiary care ctrs, miners, welders, sandblasters; Sx/Sx no specific; Dx made by culture; suspect in pts not responding to TB therapy; more severe in AIDS pts; Rx same as M.avium
🗑
|
||||
| M. scrofulaceum | common soil mycobacterium that colonizes respiratory secretions; causes chronic lymphadenitis (scrofula) w/multiple affected nodes that eventually cause draining sinuses (head/neck); Rx same as M. avium
🗑
|
||||
| Adult respiratory distress (ARD): Acute, exudative phase | rapid onset of resp failure after trigger; diffuse alveolar damage (epithelial/capillary) w/inflam cell infiltration; hyaline membrane formation; ptn-rich edema fluid in alveoli
🗑
|
||||
| ARD: Subacute, proliferative phase | persistent hypoxemia, development of hypercarbia, fibrosing alveolitis, further dec in pulm compliance and pulm HTN
🗑
|
||||
| ARD: Chronic phase | obliteration of alveolar and bronchiolar spaces and pulm capillaries
🗑
|
||||
| ARD: Recovery phase | gradual resolution of hypoxemia improved lung compliance resolution of radiographic abnormalities
🗑
|
||||
| ARD: Pathogenesis | inciting event; inflam mediators: damage to microvascular endothelium/alveolar epithelium, inc alveolar permeability results in alveolar edema fluid accumulation
🗑
|
||||
| ARD: further pathogenesis - Cellular & Humoral (comp, coag/fibrinolysis, kinin) | target organ injury from host inflam resp & uncontrolled release of inflam mediators; localized SIRS (syst inflam response syndrome); PMNs/MQs, complement, TNF, IL1b, IL6, Platelet act factor; eicosanoids (PG, Leukotrienes, Thromboxane); NO, free radicals
🗑
|
||||
| ARD: Pathology | damage to capillary endothelial cells & alveolar epithelium; permeability defect (type I pneumocyte damage and surfactant disruption); dec pulm compliance; activation of pro-inflam cascaded SIRS and compensatory anti-inflam response
🗑
|
||||
| Normal alveolar-capillary relationship | for any given membrane permeability, net fluid flux is determined by difference btw balance of hydrostatic pressures which pushes fluid out of vessels and oncotic pressures which hold fluid in the vessels
🗑
|
||||
| Cardiogenic pulmonary edema: alveolar-capillary relationship | membrane permeability is unaltered, but inc capillary hydrostatic pressure causes net fluid flux into lungs; once lymph drainage is overwhelmed, fluid floods alveoli and gas exchange deteriorates
🗑
|
||||
| Non-cardiogenic pulmonary edema: alveolar-capillary relationship | membrane permeability increaseses & eliminates differences btw capillary and interestitial oncotic pressures; promotes fluid flux into lungs at all levels of intravascular hydrostatic pressure; alveolar flooding dec lung compliance = hypoxemia of ARDS
🗑
|
||||
| Criteria for diagnosis Adult Respiratory Distress Syndrome | appropriate risk factor (sepsis, aspiration, trauma); severe hypoxemia despite O2 therapy; inc pulmonary shunt fraction; dec lung compliance; pulm edema on CXR; previously nml lungs; no evidence of heart failure
🗑
|
||||
| ARDS Stats | case fatality of 65% (90% w/in 14days); 90% require intubation by 72hrs; median onset of ARDS after predisposing event is 22hrs
🗑
|
||||
| ARDS Risk Factors | Indirect (sepsis, multiple trauma, pancreatitis, cardiopulm bypass, burns); Direct: (gastric aspiration, toxic inhalation, pneumonia)
🗑
|
||||
| ARDS Physical exam | tachypnea and anxiety (universal); Central peripheral cyanosis (depends on degree of O2 desaturation); Inspiratory rales...you will not find - wheezes, JVD, periph edema, 3rd heart sound
🗑
|
||||
| ARDS Management | maximize O2 delivery; supportive care; ID prdisposing cause; hemodynamic monitoring, mech ventilation, defend ICU complications (nosocomial infxn, stress-related GI bleeds, PE/DVT, malnutrition)
🗑
|
||||
| O2 delivery equation | (HRxSV) x Hb x 1.34 x %sat
🗑
|
||||
| ARDS Therapy Supportive Option | inc FiO2, PEEP therapy, Packed RBCs, Vol reduction (elim V/Q mismatch, dec shunt, inc O2 content, improve CO; there are adverse effects
🗑
|
||||
| Goal of mechanical ventilation | O2 sat >90%
🗑
|
||||
| MODS (multi-organ dysfunction syndrome) | organ failure is a continuum, not all or none; homeostasis cannot be maintained w/o intervention; sepsis/SIRS (temp >38C, HR>90, RR>20, PaCO2<32; WBC>12,000, Bands>10%)
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|
||||
| MODS: Epidemiology | #1 cause of death in non-coronary ICU; 13th cause of death in US; on the rise d/t antibx therapy and resistant bugs; improved ICU life support; immunossupressive drugs; organ transplants; invasive catheters/procedures; prosthetic devices
🗑
|
||||
| MODS: Pathophysiology | infxn, release of endotoxin/bacterial products; release of inflam mediators (cytokines); sepsis +/- MODS; sepsic shock +/- MODS; recovery or death
🗑
|
||||
| MODS: Pathophysiology: clinical fallout, symptoms and outcome | fallout (vasodil & vasoconst, maldistribut of blood flow, endothelial damage, myocardial dep/dilatation); symptoms (fever, tachycardia, tachypnea, HTN, MODS); recovery or death (depends on # organs involved, shock, >65); **lungs fail 1st, kidney last**
🗑
|
||||
| Who has allergies? | 90% of allergy pts can alleviate symptoms w/avoidance and oral antihistamines/nasal steroids; the other 10% includes young kids, anaphylaxis pts...do skin testing at that point
🗑
|
||||
| Comparison of pulmonary and systemic vascular pressure | the difference is 15mmHg to 100mmHg b/c of the distance and number of organs each loop needs to perfuse
🗑
|
||||
| Pulmonary arteries | low pressure; thin walls, little smooth muscle, they only need enough pressure to get to top of lungs
🗑
|
||||
| Alveolar and extra-alveolar vessels | alveolar - mainly capillaries exposed to alveolar pressure (they compress if pressure inc);extra-alveolar are pulled open by the radial traction of the surrounding lung parenchyma b/c the effective pressure around them is lower than alveolar pres
🗑
|
||||
| Pulmonary vascular resistance | (input pressure - output pressure) divided by blood flow; this allows comparison of different circulations or the same circulation under different conditions
🗑
|
||||
| Hypoxic pulmonary vasoconstriction | alveolar hypoxia constricts sm pulm aa as a direct effect of low PO2 on vascular smooth muscle; critical at birth in transition from placental to air breathing; directs blood away from poorly ventilated areas in diseased lung of adult
🗑
|
||||
| Definition of Pulmonary Hypertension | resting PAPmean >25mmHg; Exercise PAPmean >30mmHG; mild pulmonary hypertension is abnormal!
🗑
|
||||
| Three categories of pulmonary hypertension (PAH) | Presymptomatic/compensated, Symptomatic/decompensating, Declining/decompensated
🗑
|
||||
| Pulm HTN vascular pathophysiology | proliferation of intima, hyperplasia of smooth muscle, adventicial fibrosis; PVR increases and pulm artery pressure inc to maintain CO; as long as RV can compensate for resistance, the pressure continues to rise with PulmVR
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|
||||
| Pulm HTN: increased RV work load | causes RV to hypertrophy and loss of efficiency; right heart failure ensues and PAP falls as pt decompensates; failure ro maintian CO leads to symptoms of the disease, right heart dysfxn and death
🗑
|
||||
| Pathogenesis of PAH (pulm artery HTN): Risk factors | collagen vascular disease, congenital heart disease, portal HTN, HIV, drugs/toxins, pregnancy, genetic susceptibility
🗑
|
||||
| Pathogenesis of PAH (pulm artery HTN): Vascular injury | REVERSIBLE: endothelial destruction (dec NO synthase, dec prostacyclin/PG production, inc thromboxane production, inc endothelin 1 production); Vascular smooth muscle hypertrophy vasoconstriction (imparied voltage-gated K channels)
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|
||||
| Pathogenesis of PAH (pulm artery HTN): Disease Progression | IRREVERSIBLE: waning response to short-acting vasodilators; smooth muscle hypertrophy, adventitial/intimal proliferation, in situ thrombosis, plexiform lesion
🗑
|
||||
| WHO Classification of Pulmonary Hypertension | 1. Pulmonary arterial hypertension; 2. Pulmonary hypertension w/L heart disease; 3. Pulmonary Hypertension a/w lung diseases &/or hypoxemia; 4. Pulmonary hypertension d/t chronic thrombotic &/or embolic disease
🗑
|
||||
| Pulmonary Arterial Hypertension causes | idiopathic, familial, a/w coll vascular disease, congenital systemic-pulm shunts, portal HTN, HIV, drugs/toxins, other Dxs, venous/capillary occlusion or hemangiomas, persistant pulm HTN of newborn
🗑
|
||||
| Pulmonary hypertension with left heart disease causes | left sided ventricular heart disease, left sided valvular heart disease
🗑
|
||||
| Pulmonary hypertension a/w lung diseases and/or hypoxemia causes | COPD, interstitial lung disease, sleep disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude, neonatal lung disease, alveolar capillary dysplasia
🗑
|
||||
| Pulmonary hypertension d/t chronic thrombotic and/or embolic disease causes | thromboembolic obstruction of proximal pulmonary arteries, thromboembolic obstruction of distal pulmonary arteries, non-thrombotic pulmonary embolism (tumor, ova/parasites, foreign materials)
🗑
|
||||
| What are the diagnostic challenges of pulmonary hypertension? | deterimining if it is present (index of suspicion prevents delay in diagnosis, are risk factors present, order ECG for unexplained dyspnea) and what is its cause
🗑
|
||||
| Risk factors for pulmonary hypertension | family hx of dx, CT dx (mc & severe: CREST, SLE, RA); congenital heart disease, portal hypertesion, DVT/PE history, appetite suppressant/drug use, HIV
🗑
|
||||
| A critical step in the work-up of suspected PAH is the: | ECHO and Right heart catheterization; look for inc sPAP or TR jet, RA or RV hypertrophy, flattening of IV septum, small LV dimension, dilated PA; *make sure you diagnose b/f you treat*
🗑
|
||||
| What if you treat a pt w/LV disease for PAH? | vasodilation will make LV even more overloaded
🗑
|
||||
| Left heart disease | may be the mc cause of PH; may be missed (esp diastolic dysfxn) when PH is present; subtle: LAE (enlarement), LVH; think about age & underlying diseases (scleroderma, HTN, DM); normal PCW (pulm cap wedge pressure) does not exclude LH disease in some pts
🗑
|
||||
| Ventilation perfusion lung scan in pulmonary hypertension | total mismatch
🗑
|
||||
| should you use CT or MRI to exclude chronic thromboembolic pulmonary hypertension | NO...b/c these tests can miss peripheral embolisms; they focus more centrally
🗑
|
||||
| Lung disease and PH: Diagnostic challenge | usu mild, but "outliers" are seen; pts w/lung or resp disease can have concomitant PAH or other causes (LV dysfxn, TE); partition the severity of PH and severity of lung disease...which one explains exercise limitation?
🗑
|
||||
| Important PAH Treatment Goals | improve hemodynamics, exercise capacity, function, prevent clinical worsening and improve survival
🗑
|
||||
| General therapies for PAH | diuretics, warfarin (prevent future clots), O2, digoxin
🗑
|
||||
| What are the three pathways you can target in PAH? | 1. Endothelin pathway, 2. Nitric Oxide Pathway, 3. Prostacyclin (PG) Pathway; (all involved in abnml prolif and contraction of smooth muscle cells in pulm artery)
🗑
|
||||
| What are the four classes of drugs you can use in PAH? | endothelin-receptor antagonists, nitric oxide, phosphodiesterase type 5 inhibitors (viagra), and prostacyclin derivatives
🗑
|
||||
| Oral Bosentan | approved for class III and IV PAH; *dual endothelin receptor antagonist*; long-term survival benefit
🗑
|
||||
| Oral Sildenafil | for PAH: improved exercise (6min walk distance) capabilities, CO, PVR (dec PAPmean); no improvement in clinical worsening; not sure of long term efficacy
🗑
|
||||
| Epoprostenol | IV prostaglandin; rapid efficacy, useful for pts with PAH and RV failure; administered through R heart catheterization in nursing home facilities
🗑
|
||||
| Iloprost | inhaled version (6x/d) of epoprostenol; approved for class III and IV; new, possible use in combo with oral therapies
🗑
|
||||
| Pulmonary Hypertension Conclusions | systemic approach to diagnostic workup; do a right heart catheterization before therapy; there are several highly effective treatments available
🗑
|
||||
| Ventilation: definition | CO2 removal from the body by the lungs
🗑
|
||||
| Ventilatory failure | elevated PCO2 a/w respiratory acidosis
🗑
|
||||
| Impending ventilatory failure | the inability to maintain indefinately a normal blood PCO2 after the lungs have passed the fatigue threshold...this is a clinical diagnosis
🗑
|
||||
| Intubation: ET tubes w/additional lumen for removal of subglottal secretions: | decrease the occurance of ventilator associated pneumonia (VAP) by 20-40%
🗑
|
||||
| Indications for intubation | apnea, ventilatory failure, impending ventilatory failure, O2 failure, airway protection, surgery, secretions, inc intracranial pressure (ICP) - if you hyperventilate and get PCO2 down you can dec ICP
🗑
|
||||
| Negative pressure breathing | normal breaths, ex: iron lung, cuirass
🗑
|
||||
| Positive pressure breathing | mechanical ventilation: volume limited or pressure limited modes
🗑
|
||||
| Positive end expiratory pressure (PEEP) | start breathing before pt has completely exhaled; this recruits alveoli to overcome elastic force and airway resistance
🗑
|
||||
| Static compliance | affected by the lung's elasticity; = tidal volume divided by (plateau pressure - PEEP); nml = 60-100ml/cm H20; stiff lungs increase plateau pressure and lower compliance
🗑
|
||||
| Dynamic compliance | affected by airway resistance and conditions that effect static compliance; = tidal volume divided by (peak pressure - PEEP); nml = 50-80ml/cm H20
🗑
|
||||
| Control mode for mechanical breathing | time triggered, vol limited, vol cycled; no pt interaction w/ventilator; no triggering of breaths, no spontaneous breaths, preset rate and tidal vol and min ventilation; *not in current use*
🗑
|
||||
| Assist/control ventilator | time or pressure triggered, vol limited, vol cycled; preset backup rate & tidal vol (control mode); pt can trigger add'l breaths at preset tidal vol (assist mode); pt generated neg pressure trigger for assisted; pt controls Min vol; min work of breathing
🗑
|
||||
| IMV mechanical breathing | time or pressure triggered, vol limited, vol cycled; spontaneous breaths are completely done by pt (neg pressure) against continuous open gas flow; machine breaths are NOT synchronized w/spontaneous breaths by pt
🗑
|
||||
| SIMV mechanical breathing | time or pressure triggered, vol limited, vol cycled; spont breaths are completely done by pt (neg press); spont and machine breaths done against closed-on demand system & triggered by demand valve; machine breaths synched w/pt breaths
🗑
|
||||
| Pressure support mechanical ventilation | press triggured; press limited; flow cycled; preset press on pt demand (pt generates neg press); pt controls initiation & cessation of breath, tidal vol (depending on compliance and resistance)
🗑
|
||||
| Pressure control mechanical ventilation | time triggered, pressure limited, time cycles; preset pressure, inspiratory rate and time
🗑
|
||||
| Pressure limited vents w/pressure support | cycle off when flow is 25% of max flow; pressure resets and volume is variable
🗑
|
||||
| Pressure limited vents w/pressure control | time triggered; limited by pressure; give it an inspiratory time (pt will hold breath before they can release it
🗑
|
||||
| Full ventilatory support | assumes the entire responsibility (work) for breathing; PCO2 will be 35-45 if pt stops breathing spontaneously
🗑
|
||||
| Partial ventilatory support | assumes only part of the responsibility (work) for breathing; PCO2 will rise above 45 if pt stops breathing spontaneously; volume limited, pressure limited
🗑
|
||||
| Which ventilatory supports give both full and partial support? | volume limited: IMV, SIMV; and pressure limited: pressure support
🗑
|
||||
| Weaning off ventilatory support | transition from full ventilary support to partial or no ventilatory support, by which the pt progressively assumes a greater portion of the total work for breathing
🗑
|
||||
| In order to start weaning pt off ventilatory suppoer, you want to make sure they will be ok, so: | reverse the initial insult (pulm, cardiac, systemic); optimize O2 delivery; correct electrolytes; correct metabolic abnormalities; give adequate nutrition
🗑
|
||||
| Failure to wean: signs and symptoms | changes in vital signs by 10%; diaphoresis, uncoordinated respiratory effort, hypoxemia, hypercapnia, arrhythmias
🗑
|
||||
| Barotrauma vs volutrauma | pressure doesn't actually damage the lungs; alveoli become distended and damaged from too much volume administerd by positive-pressure ventilators;
🗑
|
||||
| Permissive hypercapnea | in clinical situations that call fro high airway pressures and alveolar volumes (asthma, ARDS), allow for higher PCO2 and lower pH; contraindications: cerebral dxs
🗑
|
||||
| Pneumonic findings on CXR | unilateral or bilateral; bronchopneumonia (patchy) or alveolar filling process w/dense consolidation; cavitations; pleural effusion
🗑
|
||||
| Pneumonia diagnostic tools: History | cough (>90%); sputum (66%); chest pain (50%); fever, chills, myalgias, diarrhea, HA, sore throat, rhinitis; rate of onset; season; location; travel; exposure to illness; animals; environment; immunosuppression
🗑
|
||||
| Pneumonia diagnostic tools: Physical Exam | temp; RR; intercostals/accessory mm use; rales; wheezes; rhonchi, pleural rubs; overall health for age; BP; RR; pulse, O2 sat (**vital signs provide decision making & prognostic information)
🗑
|
||||
| Pneumonia: Microbiological tests commonly available | sputum gram & acid fast stains; sputum cultures; blood cultures; pleural fluid gram stain & culture; nasal cultures for virus; antigen detection for virus (RSV, influenza); special stains for PCP
🗑
|
||||
| Pneumonia: Microbiological tests less commonly available | urine antigen detection (legionella, pneumococcus); serum antigen detection (asperigillus, histoplasma, cryptococcus); RT-PCR for virus, chlamydia, mycobacterium; serology for psittacosis
🗑
|
||||
| Types of Pneumonia | 1. Community acquired (small vol aspiration, inhalation, hematogenous septic spread, contiguous spread); 2. Aspiration (large volume a/w polymicrobial anaerobic lung infxns); 3. Nosocomial (hospital acquired; ventilator associated)
🗑
|
||||
| Inhalation of airborn organisms related to community acquired pneumonia | humans (mycoplasma, influenza), soil (fungus), animals (chlamydia psittaci, coxiella)
🗑
|
||||
| Hematogenous septic organisms related to community acquired pneumonia | right sided endocarditis (septic emboli); yersinia pestis (plague); francisella tularensis (tularemia)
🗑
|
||||
| Contiguous spread of community acquired pneumonia | amoebic liver abscess
🗑
|
||||
| Risk factors for small volume aspiration of upper airway flora | debilitated host (impaired local or systemic defenses); inc vol of aspiration (altered state of consciousness; impaired glottic/cough reflex; upper GI swallowing disorders; overdose); Inc virulence of bug (recent Abx use; chronic lung dx)
🗑
|
||||
| Pulmonary defense mechanisms | gag/cough reflex (aspiration); mucociliary clearance (CF, kartagener's syndrome); Chemical surfactant (newborns); Innate/Adaptive Immunity (alveolar MQs, PMNs - neutropenic host; Lymphocytes - HIV infxn; Immunoglobulin - myeloma)
🗑
|
||||
| Typical Community Acquired Bugs | Gram Positive Cocci (Pneumococcal pneumonia; Staphylococcus aureus); Gram Negative Bacilli (Haemophilus influenzae); Gram Negative Cocci (Moraxella catarrhalis, Neisseria meningitidis); usu colonize the posterior pharynx
🗑
|
||||
| Pneumococcal Pneumonia | strep pneumonia; nml habitat is URT; carrier rate 5-70% in kids, parents, & closed populations; Effects elderly, pts w/heart & lung dx, HIV, EtOH, cancer; Abrupt onset, fever, rigor (confusion in elderly w/o fever); dense consolidation & effusions on CXR
🗑
|
||||
| Chactacteristics of bacteremic pneumococcal pneumonia in the elderly | can be a/w no fever, no respiratory symptoms, altered mental status, volume depletion, >5days of fever on therapy
🗑
|
||||
| Treatment for Pneumococcal Pneumonia | Parenteral PCN G or oral PCN V; alternatives: erythromycin, cephalosporin, clindamycin, vancomycin
🗑
|
||||
| Haemophilus Influenzae Pneumonia | types a-f and non typable strains; Habitat is URT in most adults (esp COPD); G(-) coccobacillus w/in WBC; Causes: otitis media, sirtusitis, epiglottitis, pneumonia; CXR: lower lobe, central bronchopneumonia, pleural effusion, rare to have cavitations
🗑
|
||||
| Treatement for Haemophilus Influenzae Pneumonia | Tetracycline; Sulfamethoxazole-trimethoprim; 2nd/3rd generation Cephalosporing; Amoxicillin-clavulanic acid; Ampicillin-sulbactem; NOT ampicillin (it's b-lactamase producing);
🗑
|
||||
| Moraxella Catarrhalis | aerobic G(-) diplococci; Causes: Acute otitis media, Acuter sinusitis, Pneumonia; Predisposing factors: Alcoholism, Chronic lung disease, Humoral immunodeficiency; CXR: patchy segmental lower lobe & rarely effusions or cavitations
🗑
|
||||
| Treatment for Moraxella Catarrhalis | Tetracycline, SMX-TMP, Cephalosporins, Erythromycin, Amoxicillin-clavulanate, Ampicillin-sulbactam; (b/c most produce b-lactamase)
🗑
|
||||
| Meningococcal Penumonia (Neisseria meningitidis) | G(-) diplococci; 13 serogroups; Habitat is URT in 5-30% of adults; Causes: Pneumonia in alcoholics & military recruits; skin lesions; CXR: airspace pneumonia, bronchopneumonia, occasional effusion; rarely cavitations
🗑
|
||||
| Treatment for Meningococcal Penumonia (Neisseria meningitidis) | Penicillin, Cephalosporin, Tetracycline, Erythromycin, SMX-TMP
🗑
|
||||
| Staphylococcal pneumonia (S. aureus) | G+ in clusters; Habitat is anterior nares in 20-40% of adults; Causes: Pneumonia in post-influenza, IVDAs, nosocomial; skin lesions; CXR: usu bronchopneumonia, often bilateral, commonly cavitations/effusions; hematogenous; multiple nodules
🗑
|
||||
| Treatment for Staphylococcal pneumonia (S. aureus) | Methicillin-sensitive (Nafcillin, Oxacillin, 1st gen Cephalosporin); Methicillin-resistant (Vancomycin, Linezolid)
🗑
|
||||
| Gram Negative Rod Pneumonia | Habitat is GI tract; Inc respiratory colonization in: Alcoholics, DM, nursing homes, hospitals, recent Abx Rx, Ventilators
🗑
|
||||
| Treatment for Gram Negative Bacillary Pneumonia | Aminoglycosides (Gentamicin, Tobramycin, Amikacin); Cephalosporin; Anti-pseudomonal PCN
🗑
|
||||
| Why is it difficult to diagnose community acquired pneumonia? | (inhalation from ambient air) virulence allows few bugs to cause disease; Minimal sputum produced; May require special media; May require serological testing
🗑
|
||||
| Risk factors for inhalation pneumonia | non-debilitated hosts (mc affected); Hx of exposure (ex: geography, occupation, hobbies, animal exposure, illness in close contacts for person-person transmission or common source exposure)
🗑
|
||||
| Atypical community acquired pneumonia: Organisms | Mycoplasma pneumoniae; Legionella pneumophila; Chlamydia pneumonia; Chlamydia psittaci; Coxiella burnetti; Francisella tularensis; Yersinia pestisi; viral; fungal; mycobacterium
🗑
|
||||
| Mycoplasma pneumoniae | human reservior; 2-3wk incub; outbreaks in families w/kids or closed populations; rare if >40yo: Presentation: No symptoms, *cough*, fever, chills, sore throat, HA, tracheobronchitis, pneumonia 3-10%, GI anorexia/nausea, chest/bone/joint pain; rhinorrhea
🗑
|
||||
| Mycoplasma pneumoniae: Signs | rales, rhonchi common; Pharyngeal erythema (50%); Lung consolidation (25%); Enlarged cervical nodes (25%); Bullous myringitis (20%) - **the only infxn w/this tympanic membrane blister**
🗑
|
||||
| Mycoplasma pneumoniae: CXR and Labs | usu unilateral bronchopneumonia (>60%); usu lower lobe; few pleural effusions; NO cavitations; Most have nml WBC; hemolytic anemia is rare
🗑
|
||||
| Mycoplasma pneumoniae: Diagnosis | Cold agglutinins 1:64 in 50% (bedside levels reliable; Complement fixation (50-80% have 4x rise in titer); Culture takes 8-25 days incubation
🗑
|
||||
| Legionella pneumonia | >20sp; Natural habitat is water; Inhaled aerosolized bugs from airconditioner or water mist; Usu occurs in outbreaks (find out who else is sick); Risks (smoker, DM, immunosuppression, cancer, chronic lung/heart/kidney disease
🗑
|
||||
| Legionella pneumonia: Clinical Features | incubation 2-10days usu no URIs; abrupt onset w/high fever myalgias & HA; non-productive cough in 3days; VERY SICK; Later purulent sputum, hemoptysis, chest pain, fever >104; N/V/D (25%); mental changes (30%)
🗑
|
||||
| Legionella pneumonia: CXR and Lab Results | unilat pathcy infiltrate; progression to consolidation; bilateral later; usu lower lobes; pleural effusions are not large; **WBCs usu very high w/left shift & hyponatremia
🗑
|
||||
| Legionella pneumonia: Diagnosis | **must request special culture**Direct fluorescent Ab of sputum (70% sens, 85-95% specif); Sputum Culture (buffered charcoal yeast extract agar (BCYE) 2-7days; Serology: titer change in 3-6wks
🗑
|
||||
| Clamydia psittaci | infects birds & transmitted to humans by inhalation of dried urine/feces or respiratory secretion is aerosolized; rarely person-person transmission; any bird worker is susceptable, quarantine, vet clinic, diagnostic labs, public health inspectors,
🗑
|
||||
| Clamydia psittaci: Symptoms present in birds | anorexia, wt loss, diarrhea, ruffled feathers, weakness, inability to fly, conjunctivitis, rhinitis
🗑
|
||||
| Clamydia psittaci: Human Clinical Features | 1-6wk incubation; myalgia, fever, HA; pulm symptoms mild & late, mental changes?, splenomegaly?
🗑
|
||||
| Clamydia psittaci: CXR and Lab Findings | patchy lower lobe pneumonia, usu unilat (w/bilat common); occasional small effusions; rarely cavitations; Nml WBC, may have elevated muscle enzymes; Dx is usu by history b/c lab work/isolation of bug is dangerous
🗑
|
||||
| Chlamydia pneumoniae | Resp transmis(droplets, closed pops & families); 10-65 day incub (~31); Not seasonal, prevalent in tropical countries at young age; 90% asymptomatic; gradual onset, sore throat/hoarse, cough days-wks later, biphasic dx, pharyngeal erythema, wheeze(asthma)
🗑
|
||||
| Chlamydia pneumoniae: Lab findings | nml WBC, difficult growth on special media; chlamydia complement fixation (CF) nonspecific, Micro-IF titer
🗑
|
||||
| Treatment of Chlamydia pneumoniae | Tetracycline, Erythromycin, 2wk course; relapses may occur
🗑
|
||||
| Q Fever | d/t Coxiella burnetti; present in sheep, cattle, goats, cats (shed in urine, feces, milk, birth); infxn from inhaling dried material; 10-28day incubation; Causes: fever, HA, myalgias, late/absent cough, chest pain, N/V, endocarditis, hepatitis
🗑
|
||||
| Q Fever: CXR and Lab Findings | may be nml, usu unilateral bronchopneumonia, rare/small pleural effusion; very rare cavitations; Nml WBC, may inc liver enzymes, special media for culture; *Dx w/complement fixation serology*
🗑
|
||||
| Tularemia | d/t Francisella tularensis; G(-) bacillus; **blood borne transmission** by wild rabbits, ticks, deer flies; 2-5day incubation; cutaneous ulcer, enlarged regional node, cough, fever, chest pain; **NO respiratory symptoms**
🗑
|
||||
| Tularemia: CXR and Lab Findings | unilat patchy opacities; lower lobes; bilateral (30%), effusion (30%); nml WBC, not seen on Gram stain; **hazardous isolation; **Serology: Agglutinins 4x change >1:160
🗑
|
||||
| Plague (Yersinia pestis) | SW USA; spread from wild rodent to fleas; transmitted by bites, animal contact, inhalation, people; **Pneumonic (1* inhalation & 2* Hematogenous)**, Bubonic or Septiciemic; high mortality if not treated
🗑
|
||||
| Yersinia pestis | enterobacteriaceae; aerobic G(-) bacillus; intracellular; bipolar staining w/special stains; Highly virulent (F1 antiphagocytic capsule & LPS endotoxin);
🗑
|
||||
| Primary pneumonic plague: Pathogenesis | inhale bug, lobular pneumonia; pulm necrosis; bacteremia; multiorgan seeding/failure; sepsis; 1-4day incubation; initial symptoms are flu-like (F/C/HA/myalgias, N/V/D & abdominal pain); 2nd day (severe cough, hemoptysis, SOB, skin pupura/acral necrosis;
🗑
|
||||
| Clinical plague features: Bubonic & Septicemic | groin/axillary lymphadenopathy (bubo, may drain); versus same flu-like illness progressing to sepsis w/no adenopathy
🗑
|
||||
| Infection control of plague | pneunominc (respiratory droplet isolation - wear a mask; isolate until 48hrs treatment); Bubonic (contact isolation if buboes are draining)
🗑
|
||||
| Diagnosis of Plague | high index of suspicion necessary; no rapid tests; biplar staining of bacilli w/Giemsa stain (not gram); Take samples from blood, sputum, CSF and bubo fluid; WBC 15-20,000; Confirm w/culture, serology
🗑
|
||||
| Treatment of Plague | **Aminoglycosides are the 1st choice (streptomycin, Gentamicin)**; Tetracycline (doxycycline); Fluoroquinolones (ciprofloxacin); Chloramphenicol for meningitis
🗑
|
||||
| Post-exposure prophylaxis for Plague | oral Abx (doxycycline, ciprofloxacin for 7days); treate those exposed to initial aerosol release, asymptomatic contact of pneumonic case (household, hospital, w/in 2meters)
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| Influenza Pneumonia | underlying cardiopulm dx, tropical influenza worsens, elevated WBCs, diffuse bilateral infiltrates, 2* bacterial infxn, antiviral therapy uncertain
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| Large Volume Aspiration Pneumonia | often leads to anaerobic lung infxn; a/w GI or CNS diseases; pt unable to protect airway (altered consciousness, swallowing disorder, intestinal obstruction)
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| Anaerobic lung infxn | *putrid sputum in 50%; usu polymicrobial; CXR (dependent segment infiltrate w/several large cavities; **effusion is very common**)
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| Conditions predisposing to anaerobic lung infxn | Larger vol aspiration; 2. Lung abnormalities (sterile pulmonary infarct; bronchogenic CA; bronchiectasis; foreign body); **3. Poor dentition or carries**
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| Treatment for Anaerobic Lung Infection | Penicillin, Clindamycin, Metronidazole-penicillin; Amoxicillin-clavulanic acid; Ampicillin-sulbactam
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| Outpatient pneumonia w/o comorbidity <60yo | 1. S. pneumonia; 2. M. pneumoniae; 3. Respiratory viruses; 4. C. pneumoniae (**notice that 3 are atypical inhalation bugs); Treat w/macrolides or Fluoroquinolones (erythromycin; clarithro or azithro in smokers)
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| Outpatient pneumonia w/comorbidity and/or >60yo | 1. S. pneumoniae; 2. Respiratory viruses; 3. H. influenza; 4. Aerobic G(-) bacilli (notice that the G(-)s are creeping up the list...less atypicals; treat for strep and G(-)s w/2nd gen cephalosporin)
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| What do you prescribe if you think legionella is a concern? | macrolides/fluoroquinolone
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| Hospitalized (non-ICU) pts w/community-acquired pneumonia | 1. S. pneumoniae; 2. H. influenzae; 3. Polymicrobial (incl anaerobes); 4. Aerobic G(-) bacilli; 5. Legionella (notice anaerobes, G(-)s and legionella); Tx w/2nd or 3rd gen cephalosporin, +/- macrolide/fluoroquinolone
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| Severe hospitalized (ICU) community-acquired pneumonia | 1. S. penumoniae; 2. Legionella; 3. Aerobic G(-) bacilli; 4; M. pneumoniae (*go after the top 3...legionella has 25% death rate when hospitalized); Tx w/macrolide/fluoroquinolone + 3rd gen anti-pseudo cephalosporin
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| What are the most common bugs causing nosocomial pneumonias? | aerobic gram-negative bacilli (60-85%)
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| Most common nosocomial pneumonia bugs | Staphylococcus aureus > Pseudomonas aeruginosa > enterobacter sp > Klebsiella > Haemophilus...
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| Antibiotic stragegies for pneumonia: Old Agents | ampicillin & amoxicillin (not active against b-lactamase or atypicals); TMP-SMT (not active against atypicals); Erythromycin (not for H. influenzae or **Smokers**); Tetracycline (not for pneumococci); 1st gen cephalosporins (not for b-lactamases)
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| **Antibiotic stragegies for pneumonia: New Agents** | Amoxicillin-Clavulanate; 2nd or 3rd Gen Cephalosporins (active against b-lactamases); Azithromycin, Clarithromycin, Fluoroquinolones are ok too
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| New Macrolides: Azithromycin | food alters absorption; qday dose; adjust for liver; decreases theophylline clearance...doesn't get to sinuses b/c dose is too short you need 2-3wks of treatment; Salmonella, shigella, vibrio cholerae, e. coli
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| New Macrolides: Clarithromycin | BID dosing; not altered by food; upsets GI; dose adjust for renal; may dec theophylline clearance; S. pneumoniae, non-MRSA staph, H. influenzae, M. catarrhalis, M, pneumoniae, C, pneumonia, Legionella
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| New Agents: Fluoroquinolones | inhibits DNA gyrase; effective against G+ and (-) and many inhaled atypicals (not usu anaerobes); can dec theophylline clearance
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| Pleura | a serous membrane that covers lung parenchyma (visceral), mediastinum, diaphragm, rib cage (parietal)
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| Pleural space and pleural fluid | potential space btw parietal & visceral pleura w/film of fluid; acts as lubricant; origin is interstitial fluid from interstitial space of lung
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| Causes of pleural effusion | Inc pleural fluid formation (inc interstitial fluid in lung; inc intravascular pressure in pleura; inc pleural fluid ptn; dec pleural pressure); Dec pleural fluid absorption
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|
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| Leading causes of pleural effusions according to NEJM | CHF, Pneumonia, Cancer, Pulmonary embolus, Viral disease, Coronary artery bypass surgery, Cirrhosis w/ascites
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|
||||
| Indications for Thorocentesis | >10mm of fluid on lateral decubitus CXR; use ultrasound guidance if effusion is small or difficult to isolate; Diagnostic (all new effusions except if heart failure); Therapeutic (respiratory distress or SOB d/t pleural effusion
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|
||||
| Contraindications for Thorocentesis | coagulopathy (INR >2, platelets <25,000); Mechanical ventilation (positive pressure breathing)
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|
||||
| Thoracentesis Complications | Pneumothorax; re-expansion pulmonary edema (**don't take >1L**); Hemothorax, Infxn, Hypotension, Hepatic or Splenic puncture
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|
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| Pleural Effusions: Routine lab tests | Serum (LDH, protein); Pleural Fluid (total ptn, LDH, glucose, cell count/diff; pH on ice; Gram stain, culture, fungal stain & culture; AFB; cytology)
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| Pleural Effusions: Special lab tests | Triglyceride level & Chylomicrons (to r/o chylothorax); Amylase (to r/o pancreatitis and esophageal perforation); Adenosine Deaminase (to evaluate TB)
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| Light's Criteria for Exudates | should meet 1 of 3 criteria: 1. Pleural fluid LDH/serum LDH >0.6; 2. Pleural fluid ptn/serum ptn >0.5; 3. Pleural fluid LDH >2/3 upper limit of normal serum LDH; (it is a transudate if none of these criteria are met)
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| Transudate | results from imbalances in oncotic & hydrostatic pressure; usu low oncotic +/- high hydrostatic pressure (pulm edema/CHF; cirrhosis w/ascites; hypoalbuminemia/nephrotic syndrome, ESLD; fluid overload; peritoneal dialysis)
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| Normal pulmonary hemodynamics | net fluid flux is determined by difference btw balanced hydrostatic pressures which push fluid out of vessels; and the balance of oncotoc pressures which tends to hold fluid in the vessels
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| Cardiogenic pulmonary edema | membrane permeability is unaltered, but inc capillary hydrostatic pressure causes net flux into lungs; when lymph is overwhelmed, fluid floods the alveoli & gas exchange deteriorates
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| Transudative Effusions | usu clear straw colored, non-viscous, odorless; WBC <1000
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| Exudative Effusions | results primarily from pleura and lung inflammation or impaired lymphatic drainage of pleural space; caused by local (not systemic) factors; non-straw, bloody color, turbid, odorous
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| Exudate Causes | infection, neoplasm, pancreatitis, esophageal perforation, RA, SLE, Sarcoidosis, Wegeners granulomatosis, PE, Meig's, Chylothorax
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| Bloody exudate | cancer, PE, trauma, hemothorax
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| Cloudy/turbid exudate | chylothorax,
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|
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| Putrid odor exudate | possible anaerobic infxn
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|
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| Lymphocytosis in effusion | malignancy (50-70% lymphs); TB, sarcoidosis, RA, chylothorax (>90% lymphs)
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|
||||
| Pleural Eosinophilia | pneumothorax, hemothorax, pulmonary infarct, parasitic disease, fungal infection, drugs, malignancy, asbestos
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|
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| Why is the glucose low? <60 | RA, TB, empyema (pus from infxn); SLE; malignancy, esophageal rupture
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|
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| Empyema | pus must be removed; cannot be cured by Abx alone b/c of lack of blood supply; can lead to sepsis if untreated
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|
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| Who needs a chest tube? | presence of pus, positive gram stain, pH <7.0, LDH >1000, Hemothorax (can cause entrapped lung from coagulated dried blood that sticks to chest wall and forms fibrothorax)
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|
||||
| Types of Pneumothoraces | 1. Spontaneous (1*(PSP) in absence of clinical dx; 2* (SSP) in presence of clinical lung disease); 2. Traumatic (penetrating or blung thoracic injury); 3. Iatrogenic
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|
||||
| Management of Spontaneous Pneumothrax: Immediate Option | supplemental O2 (results in 4x dec in pneumothorax b/c most of trapped air is Nitrogen & it gets pushed out); Observation (small PSP, asymptomatic, no progression in 6hrs); Simple aspiration (70% of moderate PSP); Chest tube drainage (for all SSP)
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|
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| Prevention of Recurrence of Spontaneous Pneumothrax: Therapeutic Option | clinical pleurodesis via chest tube; talc slurry & doxycycline (irritates & scars visceral pleura to cause minor inflam and prevent further probs); VATS (stapling of bleb followed by talc pourage
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|
||||
| Causes of Secondary Spontaneous Pneumothorax | Diseases of airway; Interstitial lung diseases; Infectious diseases; Malignancy; Others
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|
||||
| Causes of Secondary Spontaneous Pneumothorax: Diseases of Airway | COPD (blebs in periphery); CF; Status asthmaticus (high pressure pushes out blebs)
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|
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| Causes of Secondary Spontaneous Pneumothorax: Interstitial Lung Diseases | Langerhans cell granulomatosis, Sarcoidosis, Lymphangioleiomyomatosis, Tuberous sclerosis, Rheumatoid disease, Idiopathic pulmonary fibrosis, Radiation fibrosis
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|
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| Causes of Secondary Spontaneous Pneumothorax: Infectious diseases | necrotizing Gram-neg pneumonia; Anaerobic pneumonia; Staphylococcal pneumonia; AIDS w/pneumocystic pneumonia; Mycobacterium tuberculosis
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|
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| Causes of Secondary Spontaneous Pneumothorax: Malignancy | Sarcoma; Lung cancer (ex: squamous cell of lung)
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|
||||
| Causes of Secondary Spontaneous Pneumothorax: Others | Catanenial (a/w women's period); Pulmonary infarction; Wegeners granulomatosis; Marfan syndrome; Ehlers-Danlos syndrome
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|
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| Coccidiomycosis (San Joaquin Valley Fever); Coccidioides immitis | d/t soil fungal arthospores inhaled in dry desert areas; highly endemic but spores blow around & travel can enhance infxn; occupational hazards (agriculture, construction, archeology); dark skin (ex: Filipinos) are more susceptible to disseminated infxn
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|
||||
| Coc-see Virulence factor | a small number of arthroconidia (alternate cells along fungal hyphae); form spherules, endospores & more spherules
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|
||||
| Coc-see infections | **60% are ASYMPTOMATIC; 35% have "Valley Fever" (mild dx w/myalgias, HA, pneumonia symptoms); 5% have severe dx (pulmonary abscess formation, liver, kidney, meningitis; desert bumps...very rare, granulation tissue masses on skin/face)
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|
||||
| Coc-see skin tests | very sensitive and specific test...BUT, it only tells if person has been exposed; **not diagnostic or therapeutic**
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|
||||
| Coc-see therapy | Fluconazole (12-18mo or indefinate for meningitis); or Itraconazole (12-18mo); or Amphotericin B (**nephrotoxic & ototoxic; monitor serum; use for immunocomp pts)
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|
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| Histoplasma capsulatum | dimorphic fungus (mycelial hyphae in environ & yeast-like in human tissue); Endemic in Ohio/Mississippi River valley; *95% are ASYMPTOMATIC w/self-limited disease (non-prod cough, low fever, chest pain, fatigue)*; affects fewer people than coc-see
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|
||||
| Histoplasmosis | 5% of infected pts develop chronic progressive lung disease, chronic cutaneous or systemic dx or an acute rapidly fatal infxn (esp if HIV+ or very young); inhalation of conidia; Diagnose w/CXR pulmonary calcification and positive skn test
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|
||||
| Causes of Histoplasmosis | a/w guano & debris from birds/bats (starlings or pigeons); occupational exposure (construction, farming, spelunking, pigeon farming)
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|
||||
| Treatment of Histoplasmosis | usu only requires supportive therapy; in HIV pts (esp w/low CD4 counts) can disseminate & involve any or all organ systems and require aggressive therapy (Amphotericin B wks-mo; Itraconazole or Fluconazole)
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| Pneumocystis carinii/jiroveci | monomorphic fungus; cannot be grown in culture; **Dx w/Methanamine Silver Stain of BAL specimen or transbronchial biopsy**; 90% of cases a/w AIDS (an AIDS defining infection)
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|
||||
| Pneumocystis Triad of Symptoms | Dyspnea on exertion, non-productive cough, low-grade fever....obviously not very specific; must get a good history
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|
||||
| Treatment for Pneumocystis | TMP/SMX w/ or w/o CCsteroids; AIDS pt prophylaxis after infection (inhaled pentamidine isethionate)
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|
||||
| Aspergillus neoformans | monomorphic; widespread filamentous fungi; causes invasive pulmonary dx when conidia or spores are inhaled; *nosocomial oubreaks occur w/contaminated air ducts*; HIV pts are at great risk; get a BAL for specimen
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|
||||
| Aspergillus treatment | Amphotericin B or Itraconazole; may need to add steroids for allergic aspergillosis
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|
||||
| Blastomyces dermatitidis | starts as a pulmonary infxn caused by inhalation of conidia; conidia transform to yeast and evades immune system by changing surface antigens
🗑
|
||||
| Blastomycosis | variable presentation (nothing or severe); dry cough, some *pleuritic pain*; hoarseness, low grade fever; symptoms mimic TB, chronic histoplasmosis or coc-see; pulmonary infxn can be fatal & spread to skin, bones GU tract or CNS
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|
||||
| Cryptococcus neoformans | encapsulated yeast spread from pigeons to humans; inhale dried spores in dusty pigeon poop; mc serious infxn is meningitis (spreads from inapparent pulmonary infxn); india ink
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|
||||
| Cryptococcus therapy | Fluconazole 6-12mo (for life if HIV+); Amphotericin B
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|
||||
| Paracocciodiodes brasiliensis | one of four truly dimorphic fungi in immunocompetent human hosts; inhaled conidiophore/spores change to yeast form that causes disease; mc in Latin America; w/o treatment fungus destroys lungs and disseminates throughout body leading to death
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|
||||
| Candida | yeast-like; normal flora of oral cavity, GI tract, sputum, vagina; infxn requires altered host defenses;
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|
||||
| Yeast versus (mold) | a fungus that grows by budding (sexual or asexual); may form hyphae in tissue; colonies are flat & moist; (A filamentous fungus; forms long hyphae strands; no budding; grows circular colonies that may be cottony or woolly)
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|
||||
| Clinical Symptoms of Candida | dermatitis, oral thrush; chronic mucocutaneous candidiasis; esophagitis; vulvovaginitis; UTI; disseminated candidiasis; endocarditis; gastrointestinal
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|
||||
| Disseminated Candidiasis | a/w pts w/malignancy, organ transplant, burns, catheters, broad-spectrum Abx use; Dx by positive blood cultures; **Treat all blood + pts whether symptomatic or not**
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|
||||
| Therapy for Disseminated Candidiasis | Fluconazole (14 days past last positive blood culture) or Amphotericin B; **remove all catheters & intravascular lines/devices
🗑
|
||||
| Pulmonary embolisms | the most clinically significant ones begin as DVT in pelvic or lower extremity veins; morbidity/mortality is unacceptably high (2nd mc cause of unexpected death in all age grps); 60% of hospital deaths; 70% of cases are not diagnosed (BAD)
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|
||||
| Causes of pulmonary embolism | blood clots from venous circulation; blood clot on right side of heart; amniotic fluid; air embolism; fat embolism; bone marrow embolism
🗑
|
||||
| Risk factors for pulmonary embolism | stasis; trauma; hypercoaguable states; prolonged bed rest/inactivity; surgery, childbirth, CVA, MI, hip fx
🗑
|
||||
| Major signs or symptoms of pulmonary embolism | dyspnea; pleuritic pain; cough; leg swelling; leg pain; hemoptysis; palpitations; wheezing; angina-like pain...only raise suspicion
🗑
|
||||
| Diagnosis of Pulmonary Embolism | clinical picture; look for risk or predisposing factors of DVT; tests (ECG, D-dimer, CXR, V/Q scan; Spiral CT; angiography)
🗑
|
||||
| Tests to detect DVT | doppler ultrasound exam on extremity; plethysmography of legs; venography of legs
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|
||||
| ECG of Acute Pulmonary Embolus | prominent S wave in lead II; Q wave & inverted T wave in lead III; Sinus tachycardia, T wave inversion in leads V1-V3; RBBB; low amplitude deflections
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|
||||
| D-dimer Assays | cross liked fibrin degradation product & plasma marker of fibrin lysis; **Great Negative Predictive value (serum <500mg/L excludes PE w/90-95% accuracy)**; but Poor Positive predictive value (overlap w/malignancy, sepsis, recent surgery or trauma)
🗑
|
||||
| Abnormalities on CXR | nml; atelectasis or parenchymal density; pleural effusion; pleural based opacity ("Hampton's Hump" w/convex medial margin); elevated diaphragm; prominent central pulmonary artery; cardiomegaly; pulmonary edema
🗑
|
||||
| Ventilation-perfusion scanning | visualizes gas exchanges in lungs using Xenon-133 & perfusion of lung w/technetium99m-labeled albumin aggregates; Does NOT directly visualize thromboembolism; The test can be: high/intermediate/low probability of PE or normal; only treat if high prob
🗑
|
||||
| Differential for positive lung CT scans | PE, infarct, hemorrhage, pneumonia, fibrosis, neoplasm, edema
🗑
|
||||
| Pulmonary Angiogram | ***the gold standard in visualizing suspected PE** look for cut-offs in vascular tree or for intraluminal filling defects; positive angiogram provides 100% certainty of obstruction in pulmonary artery; Negative angiogram: >90% certainty to exclude PE
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|
||||
| Ultrasound of Lower Extremities | duplex scanning w/compression helps detect thrombus/DVT; look for loss of flow signal, intravascular defects or non-collapsing vessels in venous system
🗑
|
||||
| Treatment of Pulmonary Embolism | O2 monitoring, fluid resuscitation for secondary RHF, inotropic drugs; Anticoagulants (heparin, oral anticoag, LMWH); Thrombolysis, Caval interruption
🗑
|
||||
| Treatment of PE: Anticoagulation | prevents clot propagation; allows endogenous fibrinolytic activity; does NOT dissolve or break up clot; dec mortality from 30-60% to <5%; IV heparin or SQ LMWH; continue until warfarin is therapeutic
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|
||||
| Treatment of PE: Warfarin | depletes Vit K-dependent clotting factors (II, VII, IX, X); PO; begin w/heparin therapy; monitor PT (prothrombin time); **continue using anticoagulation for at least 6 months**
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|
||||
| Treatment of PE: Thrombolysis | pt still requires heparin; if PE is confirmed w/angiogram or high prob V/Q; **reserved for massive PE w/circulatory shock**; Streptokinase and TPA; Catheter-directed is rarely used
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|
||||
| Treatment of PE: Inferior Vena Cava Filter (IVC filter) | used in pts that cannot tolerate anticoagulation therapy; inserted in main central vein in abdomen to block large clots from traveling into pulmonary vessels; O2 therapy requried to maintain nml [O2]
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|
||||
| Postoperative DVT Prophylaxis | if pt is not given prophylaxis, 15-30% of abdominal surgery pts will develop DVT; prophylaxis after therapy is cost-effective & reduces incidence of DVT & PE
🗑
|
||||
| Prevention of Pulmonary Embolism | Heparin (unfractionated); LMWH; Graded compression stocking (effective & few side effects); Warfarin (less effective than LMWH); Aspirin (not very effective)
🗑
|
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