Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/432

Click to flip

432 Cards in this Set

  • Front
  • Back
What is a Pulmonary embolism?
Majority usually begin as a DVT. (in lower extremity)
How many deaths result every year due to PE?
What % are recognized Post Mortem?
50,000

90%
What are the risk factors for PE?
Virchow's Triad
Venous stasis (usually from bed rest or during a major operation)
Injury (to the intima of the vein, usually smooth)
A Hypercoagulable state.
PE Predispositions;
BC pills + >35 + smoking.
PE Classic Triad;
Hemoptysis
Pleuritic CP
Dyspnea
Triad occurs in <20% of cases.
Are embolic events instantly fatal?
Yes
PE Physical Exam;
Not necessarily helpful in dx of PE. Increased resp. rate, Rales on ausculation, Increased 2nd heart sound (common), Increased HR, (sometimes) elevated temp., Px evidence of phlebitis, Cardiac gallop, Diaphoresis, Edema, Cardiac murmur, Cyanosis.
What is the most profound evidence for PE in a Px Exam?
Profound Hypoxia in the absence of underlying lung dz w/a normal CXR.
What labs should be ran for a suspected PE?
D Dimer (degradation product of fibrin) Elisa is 95% sensitive (if - then definetly - PE) & 45% Specific (if positive not necessarily PE) Latex agglutination not helpful.
What can a EKG look like for a pt w/PE?
Non specific changes, usually sinius tach.
S in I, q in III, inverted T in III classic but rarely seen.
What is Hemoptysis?
The expectoration of blood that arises from the larynx, trachea, bronchi, or lungs.
What is phlebitis?
Inflammation of a vein.
What is the test of choice (gold standard)to dx PE?
And when should it be ran?
Pulmonary Angiogram
Other screening studies are inconclusive.
Stron suspicion of PE exists.
Dx must be made w/certainty.
What findings might be on an CXR on a pt w/PE?
Atelectasis (lower lobe) & Parenchymal densities (seen in anyone), Hampton's Hump, Westermarks's Sign, Diaphragm may be elevated, Blunting of the left costophrenic angle.
What is Hampton's Hump?
Pleural based poacities w/convex medial margins, may be an indication of lung infarction.
What does a elevated diphragm reflect?
Volume loss in the affected lung.
What is a Pleural effusion?
Fluid in the thoracic cavity between the visceral and parietal pleura. It may be seen on a chest radiograph if it exceeds 300 ml.
Are pleural effusions common in pt's with a PE?
Yes, & are most often unilateral despite the fact that most clots are bilateral. They are almost always small, <15% of a hemithorax & rarely increase in size p 3days (a increase p 3-4days should raise suspician of a pulmonary infection of re-embolization).
What is a Westermark's sign?
(on CXR) A peripheral wedge-shaped density, which is a area of decreased vascularity & perfusion accompainied by an enlarged pulmonary artery on the affected side
Ventilation Perfusion Scan/PE;
Not used very much anymore (pulmonary arteriography used now) R/O dx of PE, or gives results of High, Inermediate, or Low Probability.
Ventilation Perfusion Scan/High Probability;
Detect areas of lung that are ventilated but do not perfuse
(as occurs in PE)results are reported as low, intermediate, or high probability of PE based on patterns of V/Q mismatch. A completely normal scan essentially excludes PE with nearly 100% accuracy, but a low-probability scan still carries a 15% likelihood of PE.
Helical CT Scan/PE;
Initial diagnostic study of choice, Faster, less contrast used. Less sensitive than perfusion scans (60% vs > 99%)Less specific than pulmonary arteriograms (90% vs > 95%)
Diagnostic work up of suspected PE;
D dimer(if low & low clinical probability no further work up needed) If elevated, helical chest CT(if neg US LE for DVT)If + tx(If US neg F/U clinically)if _ tx.
What is the primary anticoagulant used to acutely treat DVT & PE?
Heparin, loading dose of 5,000u then 1,000u q hr (keep PTT at 1.5-2 X control).
When risk of PE is highest bolus dose of 10,000-15,000u for pulmonary embolism may increase chance pt remain theraputic in 1st 24hrs.
What is Heparin?
A mixture of glycosaminoglycans that bind to & activate antithrombin III to inhibit further clot formation.
What is low molecular weight heparin?
Lovenox(enoxaprin) can be used in place of unfractionated heparin when there is a small PE, or diagnostic studies are inconclusive, but suspicion is high, also useful in DVT w/out PE (easier to administer).
What is warfarin?
(Coumadin) A compound that competes w/vit K & depletes vit K-dependent clotting factors (II,VII,IX, & X)Which inhibits clot formation. Advantage is that it can be taken orally.
When should warfarin therapy start if pt is on heparin therapy?
It can begin on day 1 of heparin therapy, & is monitored using the PT & a INR of 2.0-3.0 is sonsidered therapeutic.(several days of overlap of warfarin & heparin are usually required because of warfarin's mode of action)
Warfarin clotting factor production?
Because warfarin inhibits clotting factor production, the PT does not elevate until the preexisting clotting factors are consumed or degraded.
PE Management & Tx Thrombolytics;
Urokinase, Streptokinase & Tissue plaminogen activator (TPA) act by increasing existing clot lysis, they do not inhibit new clot formation.
Regarding PE, When should thrombolytics be used?
In studies comparing heparin & thrombolytics there is no survival advantage of thrombolytic therapy over heparin, current recomendations support the use of thrombolytics if the pt is in shock.
What other methods can be used for Management & Tx of PE?
Pressure stockings, Early ambultaion after sugery, Use of sequential compression during surgery, Small filtration devices can be placed w/in the lumen of the Vena Cava to prevent migration of the pulmonary emboli.
What is Cor Pulmonale?
Right ventricular enlargement secondary to a lung disorder that produces pulmonary artery hypertension. Uaually chronic but may be acute & reversible.
What is the cause of acute Cor Pulmonale?
Massive pulmonary emboli.
What is the cause of chronic Cor Pulmonale?
COPD, chronic pulmonary emoli, pneumoconiosis, pulmonary fibrosis, primary pulmonary hypertension & other conditions.
Cor Pulmonale Pathophysiology;
Directly caused by alterations in pulmonary circulation that lead to pulmonary arterial hypertension, thereby increasint the mechanical load on the right ventricle emptying.
Cor Pulmonale Symtoms;
Dyspnea on exertion (most common), syncope or easy fatigue w/exertion, chronic productive cough, wheezing respirations, RUQ pain (liver backs up), dependent edema (more difficult for extremeties to drain).
Cor Pulmonale Signs;
Cyanosis, clubbing, distended neck veins, right ventricular heave, tricuspid insufficiency or pulmonic insufficiency mumurs, s4,s3 gallop, prominent lower sternal epigastric pulsations, enlarged & tender liver, edema.
Cor Pulmonale Lab studies;
Polycythemia often present due to COPD.
Arterial O@ sat <85%, PCO2 may or may not be elevated.
Cor Pulmonale EKG;
Big prominent P waves, RAD, Low voltage, Supraventricular arrhythmias, right ventricular hypertrophy (uncommon)
Cor Pulmonale Chest X-ray;
Presence of parenchymal dz
Prominent right ventricle (may show)
Enlarged pulmonary artery (may show)
Cor Pulmonale Echo;
Normal LV & RV dilation.
What is the most specific test for pulmonary emboli?
Pulmonary angiography
Cor Pulmonale Right heart cath;
Will give difinitive dx but usually used to exclude LV failure.
In the early stages what usually diagnoses Cor Pulmonale?
Radiologic, Echocardiographic or EKG evidence.
Cor Pulmonale complications;
Right ventricular heart failure.
Atril fib
Cor Pulmonale Management;
Tx is directed at pulmonary process responsible for tight heart failure;
O2, fluid restriction, salt restriction, & diuretics are the mainstays for tx.
Cor Pulmonale Prognosis;
Same as underlying pulmonary dx.
Life expectancy is 2-5yrs p signs of CHF appear.
It is significantly longer when uncomplicated emphysema is the underlying cause.
Name some types of Interstitial Lung Disease;
Pulmonary fibrosis, Pneumoconiosis (coal workers lung dz), Asbestosis, Silicosis, Beryliosis, Sarcoidosis.
What is Interstitial Lung Disease?
The end result of several nininfectious & nonmalignant processes. May present acutely, intermittently, subacutely or chronically (often).
What are the 2 primary pathways of Interstitial Lung Disease?
Granulomatous
Inflammation & fibrosis.
What is Granulomatous Interstitial Lung Disease?
Accumulation of T-lymphocytes, macrophages, & epitheloid cells into discrete structures (gramulomas) in the primary parenchma. Can progress to fibrosis but usually mild symptoms that respond to tx.
What is the usual cause of Granulomatous Interstitial Lung Disease?
Sarcoid or a hypersensitivity pneumonitis.
What is Inflammation & fibrosis, Interstitial Lung Disease?
Initial injury to epithelium & alveolar walls. Chronic inflammation can spread to adjacent tissues & cause interstital fibrosis. Irreversible scarring (fibrosis) of alveolar walls, airways or vasculature is worst outcome (progressive & leads to significant physiologic impairment, poor gas exchange).
Interstitial Lung Disease S/Sx;
Progressive extertional dyspnea, Persistent non-productive cough, Fatigue & wt loss, (rarely wheezing, CP, or hemoptysis).
Interstitial Lung Disease PE;
Usually non-specific, Tachypnea, Bi-basilar inspiratory dry crackles, Rarely rhonchi, (Late in dz may have signs of Cor Pulmonale).
Interstitial Lung Disease Labs;
ANA
RE
LDH increased in most
Interstitial Lung Disease EKG;
RAD
Right heart strain
Cor Pulmonale
Interstitial Lung Disease Echo;
Right Vent Dilation
RVH
Pulm HTN
Interstitial Lung Disease CSR;
Bibasilar reticular (lace like) pattern, Nodular pattern, Poor correlation to actual clinical dz progression, Small cystic spaces/honeycombing indicates progressive fibrosis (poor prognosis), Generally non-specific (usually read as interstitial pattern).
Interstitial Lung Disease CT;
Very useful to stage progression & plan biopsy.
Interstitial Lung Disease Spiromentry;
Measures extent of lung involvement (reduced total lung capacity, FEV% normal)
Interstitial Lung Disease ABG;
Shows hypoxemia
End stage elevated PCO2
Interstitial Lung Disease Biopsy;
Can find etiology & help w/tx.
Interstitial Lung Disease Cardiac Stress Testing;
Documents difference between resting & exertional hypoxia & is useful to follow dz progression & response to tx.
Interstitial Lung Disease Tx;
Course is variable, Progression is insidious, Can't reverse fibrosis so goal is to limit scarring & inflammation, O2 if hypoxic, Glucocorticoids mainstay (but not real helpful), Cyclophosphamide & & azathioprine occasionally tried, Methotrexate & other immune modulating drugs occasionally used, Lung transplant (for end stage).
(Interstitial Lung Disease) Idiopathic Pulmonary Fibrosis Differentiate;
Important to differentiate from other causes of fibrosis.
(Interstitial Lung Disease) Idiopathic Pulmonary Fibrosis S/Sx;
Exertional dyspnea, nonproduvtive cough, inspiratory crackles (may have clubbing)
(Interstitial Lung Disease) Idiopathic Pulmonary Fibrosis Tests;
CT:patchy basilar, subpleural reticular opacities.
PFT:restrictive pattern
Poor exercise tolerance
(Interstitial Lung Disease) Idiopathic Pulmonary Fibrosis Clinical course;
Varies
5yr survival rate 40%
(Interstitial Lung Disease) Idiopathic Pulmonary Fibrosis Tx;
Immune modulating drugs used but no evidence that they improve survival or quality of life.
Lung transplant for end stage (several criteria for transplant pts)
(Interstitial Lung Disease)Pneumoconiosis describe?
Inflammation of the lungs leading to fibrosis caused by inhalation of dust related to various occupations. (Coal dust is common cause, additive effects w/smoking; rapidly advancing COPD)
(Interstitial Lung Disease) CXR simple coal miners pneumoconiosis;
Early: small, irregular ipacities (reticular)
Later: small, rounded, regular opacities 1-5mm in diameter (nodular)
Calcifications unusual
(Interstitial Lung Disease) Pneumoconiosis complicated dz CXR findings;
Nodules from 1cm to entire lobe (usually in superior 1/2 of lung)
Significantly reduced diffusing capacity.
(Interstitial Lung Disease)Pneumoconiosis Tx;
(complicated dz has poor prognosis)
Same as for other causes of pulmonary fibrosis.
Mild dz treated as COPD
More severe will involve use in immune modulating drugs.
(Interstitial Lung Disease)What is Asbestosis?
A generic term for several different forms of mineral silicate fibers. Used extensively in 1940's to 1970's
(Interstitial Lung Disease)What are the major dzs caused by asbestos?
Pulmonary fibrosis & CA of the respiratory tract & pleura.
(Interstitial Lung Disease)
What is asbestosis?
Diffuse interstitial fibrosing dz of the lung that is directly related to the intensity & duration of exposure. (clinically resembles other forms of diffuse interstitial fibrosis)
(Interstitial Lung Disease) What are the risk factors of asbestosis?
Usually moderate to severe exposure that has taken place for at least 10yrs prior to sx appearance.
(Interstitial Lung Disease)
Asbestosis Spirometry;
Reveals restrictivie pattern w/decrease in lung volumes.
(flow rates are not impacted as much as would be predicted by the volume restriction)
(Interstitial Lung Disease)
Asbestosis CXR findings;
Pleural plaques, thickening or calcification along parietal pleura, lower lung fields or cardiac border. (indicate past exposure not impairment) may have effusions. Irregular or linear opacities 1st noted in the lower field & spreading cephalad as the asbestosis progresses (occasionally indistinct hrt boarder or ground glass appearance)
(Interstitial Lung Disease)
Asbestosis Lung Cancer (squamous cell carcinoma or adenocarcinoma);
15-19 yrs from exposure to onset.
Marked increase in smokers
(Interstitial Lung Disease)
Asbestosis Lung CA (Mesothelioma);
80% of cases have some relation of asbestos exposure. Plural & Peritonea, no association w/smoking Short term exposure 1-2yrs can present in 20-25yrs, Peak incidence 30-35yrs p exposure. 50% metastasize but death usually due to local invasion. (Effusions common).
(Interstitial Lung Disease)
Asbestosis Tx;
No specific therapy, Must stop smoking, Supportive care as in other causes of pulmonary fibrosis, CA tx is type specific.
(Interstitial Lung Disease)
What is Silicosis?
Free silica (SiO2) or crystalline quartz inhalation. 1.2-3million persons in USA. Progressive pulmonary fibrosis occurs after many years of exposure in a dose response pattern
(Interstitial Lung Disease)
Silicosis Risk Factors;
Acute silicosis can develop 10mos of intense exposure to silicates. Mining, stone cutting, foundry work, granite quarry, sandblasting in confined spaces, tunneling through rock w/a high quartz content, manufacture of abrasive soaps, (fine dust).
(Interstitial Lung Disease)
Silicosis Prognosis;
Rapidly fatal in < 2yrs.
(Interstitial Lung Disease)
Silicosis Acute CXR findings;
Profuse miliary infiltration or consolidation.
(Interstitial Lung Disease)
Silicosis Chronic (after 15-20yrs) CXR findings;
Small rounded opacities in the upper lobes, Retraction & hilar adenopathy, Calcification of hilar nodes (classic eggshell pattern) Reticular pattern of irregular densities uniformly present in the upper lobes.
(Interstitial Lung Disease)
Silicosis Progressive CXR findings;
Coalescence of nodules & formation of irregular masses >1cm, can become very large.
(Interstitial Lung Disease)
Silicosis Spirometry findings;
Significant impairment, Restrictive & Obstructive, Late ventilatory failure.
(Interstitial Lung Disease)
Silicosis Complications;
Increased risk of acquiring TB & other atypical mycobacterial infections.
(Interstitial Lung Disease)
Silicosis Tx;
Same as for any other Interstitial Lung dz.
(Granulomatous Lung Dz)
Berylliosis Etiology;
Beryllium may produce a acute pneumonitis or chronic granulomatous dz (more common). 2-15yrs of exposure to manifest dz.
What is Beryllium?
Used in manufacture of alloys, ceramics, high-tech electronics, & early fluorescent lights (1950's)
(Granulomatous Lung Dz)
Berylliosis PE;
PFT usually shows restrictive dz.
Clinical picture very similar to sarcoidosis but beryllium levels are elevated.
(Granulomatous Lung Dz)
Sarcoidosis Patho?
A chronic multi-system disorder of unknown etiology. Characterized by accumulation of T-lymphocytes & mononuclear phagocytes, epitheliod granulomas & derangement of normal tissue architecture. Exaggerated T-helper 1 lymphocyte immune process.
(Granulomatous Lung Dz)
Sarcoidosis dz course;
Can involve any part of the body, but most commonly the lung. Maybe acute or subacute, but is commonly chronic, waxing & waning over many years. Environmental trigger of exaggerated immune respones suspected but antigen not identified.
(Granulomatous Lung Dz)
Sarcoidosis Epidemaology?
10-40 per 100k, 10:1 black to white in USA, but overall evenly distributed worldwide. Favors non-smokers, presents between age 20-40.
(Granulomatous Lung Dz)
Sarcoidosis S/Sx;
Onset over weeks (20-40%) or months (40-70%).
(Granulomatous Lung Dz)
Sarcoidosis S/Sx of dz onset over weeks;
Fever, Fatigue, Anorexia, Wt loss, Cough, Dyspnea, Vague retrosternal discomford, Polyarthritis, Erythema Nodosum (same type of rash as coxicidial mycosis)
(Granulomatous Lung Dz)
Sarcoidosis S/Sx of dz onset over months;
Respiratory complaints w/out constitutional Sx, Dyspnea on exertion & dry cough, Dry rales.
This type develops chronic sarcoid w/permanent damage to lung & in 10% other organs (hrt, eye, CNS)
(Granulomatous Lung Dz)
Sarcoidosis CXR findings;
90% will have a abnorman CXR. Bilateral hilar adenopathy is hallmark, Diffuse parenchymal changes consistent w/interstitial lung dz, Occasionally eggshell calcification of hilar nodes, May see granulomas.
(Granulomatous Lung Dz)
Sarcoidosis Lab Findings;
Angiotensin converting enzyme elevated in 66% of pts, Hypercalcemia occasionally, Eosinophilla, Increased ESR, Biopsy via fiberoptic brochoscope; Noncaseating granulomas, increased # of Th1 subset of CD4 T-lymphocytes.
(Granulomatous Lung Dz)
Sarcoidosis PFT findings;
Normal to increased FEV1/FVC ratio, Decreased total lung volume, Decreased diffusing capacity.
(Granulomatous Lung Dz)
Sarcoidosis ABG findings;
Mild hypoxemia
Mild, compensated hypocarbia
(Granulomatous Lung Dz)
Sarcoidosis Tx;
Main delemma is when to tx; Clears spontaneously 50%, Usually observe 2-3mos tx if not better.
Mainstay glucorticoids (Prednisone 1mg/kg x 6wks, then taper over 3mos)
2nd line Methotrexate
(Granulomatous Lung Dz)
Sarcoidosis Prognosis;
Overall good; 50% resolve spontaneously. 50% have mild permanent organ dysfunction, usually; mild, stable & rarely progresses. 15-20% will have active dz or recur intermittantly. 10% will die from dz.
What is influenza?
Acute respiratory infection w/influenza, a virus causing fever, coryza, cough, H/A, malaise, & inflamed respiratory mucous membranes.
What is coryza?
An acute inflammation of the nasal mucosa accompanied by profuse nasal discharge.
Influenza strains?
A, B, or C. Only 1 strain of influenza B is recognzed. 'A' strains are recognized by hemagglutinin & neurominidase (determines how virus spreads & replicates) Mutations of HA & NA result in antigenic drift.
What is antigenic drift?
A minor change in the protein marker or antigen on an organism. Small changes in the antigenic surface markers of some microorganisms (such as the influenza virus) occur from year to year. Vaccinations against the virus are adapted annually to combat these changes and prevent epidemic infection.
Influenza Epidemiology?
Widespread sparadic respiratory illness during fall & winter q year. Epidemica q 2-3yrs. B strains usually less virulent than A strains. Highest in school aged children their contacts, & chronic illness.
How is influenza spread?
Airborne droples, person to person or contact w/contaminated items.
Influenza risk factors?
COPD, Valvular hrt dz, Pulmonary edema, Women in 3rd trimester, Elderly, Very young, Bedridden.
Influenza S/Sx;
48hr incubation w/abrupt onset, chills, fever (102-103)sudden onset, prostration & generalized aches & pain (back of legs), H/A w/photophobia, scratchy sore throat, substernal burning, nonproductive cough, coryza.
What is prostration?
Absolute exhaustion.
What is coryza?
An acute inflammation of the nasal mucosa accompanied by profuse nasal discharge.
Severe Influenza S/Sx;
Bloody sputum, warm & flushed, Reddened mm in mouth (no exudate), Eyes burn & watering (no exudate), Nausea & vomiting in Peds, Weakness, Sweating, & fatigue may persist for several days to weeks.
Influenza when do acute S/Sx usually subside?
2-3 days.
Influenza Complications;
Hemorrhagic bronchitis & Pneumonia, Death in severe cases of pneumonia, 2ndary bacterial infection of the lungs. (Encephalitis, myocarditis & myoglobinuria are infrequent complications)
What microbes are responsible for secondary bacterial infection of the lungs in influenza?
Pneumococcal or Staphylococcal.
Influenza diagnostic tests & lab findings;
Dx is clinical, no routine testing are recomended or used. Uncomplicated Influenza leukocytes are normal. Fever & severe constitution sx differentiate the flu from common cold, X-ray may be normal.
Influenza D/Dx;
Parinfluenza
RSV
Rhinoviruses
Echoviruses
Influenza Prognosis;
Healthy pts demonstrate lingering effects for weeks p the acute illness. Severe illness may require hospitalization especially if pt is high risk (very young or very old w/comorbidities, compromised immune system) Mortality from pneumonia & Influenza 1 of the 10 leading causes of death in US (>20,000 q yr)
Influenza Prophylaxis;
Vaccinate in the fall, Immunity in 2 wks,
What types of Influenza vaccines are available?
Traditional IM vaccine (fluzone) not live.
Attenuated virus given intranasally (Flumist) Live Virus.
Who should get the Influenza vaccine?
All adults >65
Anyone w/high risk.
Women who will be in their 3rd trimester durning winter mos.
People who provide medical & nursing care.
What are the condrindications to the IM Influenza vaccine?
Allergy to eggs.
Acute neurologic disorder.
What are the condrindications to the intranasal influenza vaccine?
(live virus)
Active infection, allergy to eggs, hx of Guillain-Barre syndrome, asthma, bronchospasm, pregnancy, DM, & renal dysfunction.
What antiviral drugs are available for influenza?
Amantadine & Rimantadine (will shorten the course & lessen the effects)
Effective against A strain,
Adult dose 100mg BID
Elderly 100mg qd
Can be used in children.
What is the tx for influenza?
Symptomatic;
Rest, Hydration, Influenza antiviarals, antipyretics, analgesics, nasal decongestant, steam inhalation.
What is a antipyretic?
An agent that reduces fever.
What is Respiratory Syncytial Virus?
RSV, lower respiratory tract viral illness (including bronchiolitis & pneumonia) in infants & young children.
What are Respiratory Syncytial Virus risk factors?
Premature infants (can be fatal) Less severe manifestation in older children & adults. (one of the most important causes of lower respiratory tract illness) Thought to be the cause of SIDS w/resp dz.
Respiratory Syncytial Virus Etiology;
RNA virus (resembles influenza & parainfluenza viruses) Outbreaks in winter or early spring. Increases morbidity from bronchitis & pneumonia. Poor protective effect of serum antibody (severe infections)
Respiratory Syncytial Virus S/Sx;
Vary w/age, previous exposure & underlying dz.
Dyspnea, Cough, Wheezing appearing several days p upper resp signs including fever, Apnea, Bronchopneumonia & bronchiolitis on X-ray.
Respiratory Syncytial Virus lab findings;
Leukocyte ct normal, may have elevated granulocytes.
Respiratory Syncytial Virus S/Sx in older children & adults;
(accounts for 15% of hospitalizations for exacerbation of chronic bronchitis)
Afebrile
URI
Influenza
Respiratory Syncytial Virus D/Dx;
Isolated from respiratory secretion, enzyme linked immunosorbent assay to detect RSV antigens is convenient & timely.
Respiratory Syncytial Virus Tx;
Mild infections resolve spontaneously.
Severe dx in infants & children; Hospitalization, ABGs, O2 tx, Respiratory support.
Ribavirin (reduces shedding & accelerates recovery) Aerosolized tx 3-5 days.
What is Acute Laryngotracheobronchitis?
Croup
Acute viral inflammation of the upper & lower respiratory tracts.
What are the characteristics of Acute Laryngotracheobronchitis?
Inspiratory stridor
Subglottic swelling
Respiratory distress that is most pronounced on inspiration.
What age group is Acute Laryngotracheobronchitis most prevalent in?
Children 6mos to 3yrs
What are the major pathogens that cause Acute Laryngotracheobronchitis?
RSV
Influenza B
Adenovirus
When are outbreaks of Acute Laryngotracheobronchitis most common?
Seasonal outbreaks;
Parinfluenza fall
RSV & influenza in winter & spring
How is Acute Laryngotracheobronchitis spread?
Airborne route or contact
Acute Laryngotracheobronchitis etiology;
Croup produces inflammation of laryx, trachea, bronchi, bronchioles, & lung parenchyma (subglottic structures). Swelling & inflammatory exudate most pronounced in subglottic region, this leads to; Dyspnea & possibley hypercapnia, & Atelectasis.
What is hypercapnia?
An increase in the partial pressure of carbon dioxide in the blood. (cerebral vasodilation can occur)
What is Atelectasis?
A collapsed or airless condition of the lung.
What are possible secondary conditions to Acute Laryngotracheobronchitis?
Parenchymal pulmonary infection
What is parenchyma?
The essential parts of an organ that are concerned with its function in contradistinction to its framework.
Acute Laryngotracheobronchitis S/Sx;
Preceded by URI, Barking, spasmodic cough, hoarseness, Tachypnea, Tachycardia, retractions, Harsh inspiratory stridor, prolonged inspiration & stridor w/ some expiratory rhonchi & wheezes, breath sounds may be dimished (atelectasis) Fever (50%), imporvement in AM worsens PM.
What lab findings would you expect w/Acute Laryngotracheobronchitis ?
Marked leukocytosis w/increased PMNs.
ABGs; Hypoxemia +/-hypercapnia.
Acute Laryngotracheobronchitis D/Dx;
Epiglottis (pt appears toxic)
Bacterial tracheitis
Foreign body
Diphtheria
Retropharyngeal abscess
Acute Laryngotracheobronchitis Tx;
Most can be tx at home. Well hydrated, Rest, Humidification (cold), Tylenol or motrin. Increasing resp distress, tachycardia, fatigue, cyanosis or dehydration need hospitaliaztion.
Acute Laryngotracheobronchitis Tx of hopitalized pt?
ABGs, humidified O2 (to loosen secretion & support O2) Intubated (hypercapnia, fatigue), Nebulized racemic epi (effects transient) Dexamthasone, ABX are rarely indicated.
What is Bronchiolitis?
Acute viral infection of the lower resp tract affecting infants & young children.
What are the charastics of Bronchiolitis?
Respiratory distress, expiratory obstruction, wheezing & crackles.
Bronchiolitis epidemiology;
Occurs in epidemics in children <18mos, Peak incidence in infants <6mos. Annual incidence in 1st year of life, 11:100 children.
What Virus' usually cause Bronchiolitis?
RSV, parainfluenza 3 virus, Influenza A & B, Parinfluenza, Adenovirus.
What is the action of the virus in Bronchiolitis?
Virus spreads from upper resp tract to med & sm bronchi & bronchioles→Epithelial necrosis.
What causes obstruction in Bronchiolitis?
Edema & exudate.
Expiration→air trapping in alveoli→atelectasis.
Bronchiolitis S/Sx;
Preceding URI, Rapid onset of resp distress, tachypnea, tachycardia, hacking cough, ↑ distress w/circumoral cyanosis, deepening retractions & wheezing, lethargy, +-Fever, Dehydration, resp acidosis, hyperresonant chest on precussion, prolonged expriation, crackles.
What is circumoral cyanosis?
Central cyanosis
central cyanosis-A bluish discoloration of the mucous membranes in the mouth, indicating hypoxemia and respiratory failure.
What would you expect to find on a CXR of a pt w/Bronchiolitis?
Hyperinflated lungs, Depressed diaphragm, Prominent hilar markings, Infiltrates.
What lab findings would be expected for Bronchiolitis?
2/3 have WBC 10,000-15000/ul
BUN & electrolytes may reflect dehydration.
ABGs show hypoxemia.
Viral isolation (immunoflourescence & enzyme linked immunosorbent assay for RSV)
Bronchiolitis D/Dx;
Asthma (more likely in children >18mos w/previous hx of sx.
GERD
Foreign body aspiration.
Bronchiolitis Prognosis;
Recovery in 2-5days, Mortality rate is <1% w/adequate medical care.
What are the indications to hospitalize a pt w/Bronchiolitis?
Increasing resp distress, cyanosis, fatigue & dehydration.
Co-morbidities that put a child at risk requires more diligent f/u & possible hospitalization.
Bronchiolitis tx;
Most pts can be tx at home.
Nebulization, ribavirin & ABX (if secondary infection is present)
What tx are contraindicated or have no benefit for a pt w/Bronchiolitis?
Corticosteroids (no benefit)
Sedatives (contraindicated)
Bronchodilators (usually ineffective)
What is ribavirin?
An antiviral agent used to treat respiratory syncytial viral infection and hepatitis C.
What is the tx of a pt admitted for Bronchiolitis?
Recognize & tx hypoxemia. ABGs, PaO2<60mmHg tent face mask w/30-40% O2, Intubation (if indicated), Postural drainage, Trachal suctioning, Humidified O2, Nubulization, Hydration (PO or IV)
What is Postural drainage?
A passive airway clearance technique in which patients are positioned so that gravity will assist the removal of secretions from specific lobes of the lung, bronchi, or lung cavities.
What is Pertussis?
Whooping Cough, Acute highly communicable bacterial dz, caused by bordetella pertusis.
What are the characteristics of Pertussis?
Paroxysmal or spasmodic cough that usually ends in a prolonged high pitched, crowing inspiration (The Whoop).
What is a Paroxysmal cough?
A persistent cough occurring with a sudden onset.
What is Paroxysmal?
Occurring repeatedly and without warning.
Pertussis Epidemiology;
Endimic throughout the world, occurs at all ages, 38% occur in infants <6mos, 71% occur in peds <5yrs
Pertussis Etiology;
Nonmotile, gram-negative coccobacillus, Sprayed in the air w/coughing, Contact w/contaminated articles is rare, 1 attack does not confer natural immunity.
Pertussis S/Sx;
Incubation 7-14 days
Invades mucose of nasopharynx, trachea, bronchi & bronchioles ↑ the section of mucus, which is initally thin, then becomes very tenacious.
What are the different stages of Pertussis?
Catarrhal
Paroxysmal
Cnovalescent
Describe the S/Sx of Catarrhal stage of pertussis;
Insidious, Sneezing, Lacrimation, Coryza, Anorexia, Listlessnes, Hacking nocturnal cought & becomes diurnal, fever is rare.
What is Insidious?
Of gradual, subtle, or indistinct onset; said of some slowly developing diseases.
What is diurnal?
Happening in the daytime or pert. to it.
Describe the S/Sx of the Paroxysmal stage of pertussis;
P 10-14days, 5-15 more rapidly consecutive forceful coughs during a single expiration followed by a whoop, a hurried deep inspiration, Normal breaths than another episode of coughing ending w/a whoop, Viscid mucus, vomiting p coughing d/t viscid mucus, Choking infants d/t viscid mucus.
Describe the S/Sx of the Convalescent Stage of pertussis;
Withing 4wks, Paroxysma not as frequent or severe, other sx decreased, pt looks & feels better, duration 7wks, Paroxysmal coughing may recur for months especially when induced by irritation from a URI.
What are the complications of pertussis?
Asphyxia in infants, Bronchopneumonia (may be fatal), Interstitial & subQ emphsema & pneumothorax (uncommon) from ↑ intrathoracic pressure, Convulsions in infants, Hemorrhage into the brain, skin, MM, Cerebral hemorrhage or edema (→Mental retardation or spastic paralysis)
What tests should be ran & what results are expected for pertussis?
Cultures of nasopharyngeal secretions (especially in catarrhal & early paroxysmal stages). Special collection w/cotton swab on zinc coated wire, Bordet-Gengou or charcoal agar medium to inhibit overgrowth by other flora, Fluorescent antibody testing, Parapertussis differentiated by culture or flourescent antibody technique.
Pertussis Prognosis;
<2yr mortality 1-2%, Most deaths are from bronchopneumonia or cerebral complication, Elderly & very young have a higher risk for complications.
Pertussis Tx of choice;
Erythromycin estolate 12.5mg/kg PO q6hrs (starting during the incubation to diminish infectivity to others & aborting infection in contacts.
Pertussis Tx;
Hospitalization for serious infection (especially infants) Sm freq meals, IV hydration, Suction, O2, Minimize stimulation in infants, Expectorants, cough suppressant & mild sedation are questionable. Theophylline, albuterol & corticosteroids (controversial tx)
Pertussis ABX Tx;
Catarrhal stage may avert dz, p paroxysmal stage started ABX have no discernible effect, but recommended to limit spread, Erythromycin 40-50mg/kg q 5hrs X 14days.
What is Tuberculosis?
A chronic, recurrent infection, most commonly in the lungs.
Tuberculosis Etiology;
Caused by Mycobacterium Tuberculosis, M bovis or M aficanum. Inhalation of organism (droplet) Can float in the air for several hours.
Tuberculosis Epidemiology;
In the US is prevalent in; people >70, 2:1 blacks to whites, Immigrants, HIV, IV drug users.
Tuberculosis Initial Stage Pathogenisis;
Active at any age, Clinical TB can occur in any organ, most often Apical areas of the lungs, occurs q 1-2yrs p initial infection, May activate p onset of DM, Stress, corticosteroids, HIV. Simon foci(scars in apical areas)
Tuberculosis Latent or Dormant Stage Pathogenisis;
Typically occurs in Apex of lungs, Illness may manifest itself when some other dx facilitates its reactivation of infection.
Tuberculosis S/Sx;
Asymptomatic & Vague, Fever, Cough, Mucus on rising, Dyspnea, Wt loss, Hempotysis (late in dz).
Tuberculosis regarding the elderly;
They are easily overlooked.
Spread to others quickly (SNF)
Tuberculosis regarding HIV pts;
Common & rapid
Pleural TB Patho;
Pleural pulmonary lesion ruptures→effusion of infected material, may seed ther organs.
What are some of the reasons for the difference of dz course w/Tuberculosis?
Inoculum, Virulence of organism, Competence of host, presence of other dz, Rapid among blacks & American indians, Whites more chronic dz without serious illness.
What is Inoculum?
A substance introduced by inoculation
Tuberculosis CXR findings;
Multinodular infiltrate above or behind the clavicle-recrudescence (reactivation of a latent or dormant site of old TB infection.
Younger pts w/new infection between middle & lower lobe.
What tests could be ran to Dx tuberculosis?
AFB (acid fast bacilli on smear) Bronchoscopy w/biopsy, Throacentesis of pleural fluid, WBC, pH, histologic eval & culture. PPD.
Define prophylaxis;
Observance of rules necessary to prevent disease.
Tuberculosis PPD describe;
0.1ml intradermal injection, Induration of >10mm usually +, Does not indicate activity of infection, May be - in HIV or elderly pts (don't have strong enough immune sys to present +)
What should be done for a pt w/a + PPD?
If no active dz start prophylaxis tx.
If test + & symptoms of active dz are presesnt (x-ray changes) treat w/combination therapy.
Describe the 2 step test;
If 1st test is - repeat 1-3wks later, if + it is a booster reaction (prevents from providing unnecessary meds next time pt tests + for PPD)
What is BCG?
Vaccine made from attenuated strain of M. bovis, used in developing countries w/high rate of TB, May cause a + PPD. (recommendation is to tx these pt w/+ PPD like they are + for TB)
What is the prophylaxis tx for a tuberculosis pt?
Isoniazid (INH)300mg/day for 6-9mos
Children 10mg/kg/day
Usually noninfectious w/in 10-14 days of tx
(usually don't isolate from family, damage is already done)
Who should recieve prophylaxis tx?
Pts whose PPD converted from - to +w/in the previous 2yrs, Elderly >15mm & not a booster reaction. Small peds, HIV 10mm, IDDM, anyone who has recently converted & is at risk for complications.
Tuberculosis tx;
Goal: cure dz & limit dz spread, Have to take the full course, Single med is used when clinical dz is absent, Pts w/+ smears & extrapulmonary TB uses at least 2 drugs (INH & rifampin) for 9mos.
(Tuberculosis Tx)
What is Isoniazid?
(INH) single most useful & least expensive med for TB, Very effective when given w/rifampin, Safe during pregnancy.
What is agranulocytosis?
An acute disease marked by a deficit or absolute lack of granulocytic white blood cells (neutrophils, basophils, and eosinophils).
What are the adverse reaction of Isoniazid (INH)
Allergy; rash, drug fever, anemia & agranulocytosis. (liver injury rare but ↑w/age)
Anorexis, nausea, vomiting, jaundice, Peripheral neuropathy (tx w/vit B), Decrease dilantin dose.
What are reasons to stop Isoniazid (INH)?
Jaundice is a sign of Hep toxicity d/c med.
If transaminase (AST)is >500 d/c med (may restart at a smaller dose & see if pt tolerates)
(Tuberculosis Tx)
What is Rifampin?
(mircle drug) 600mg qd (adult)
Safe w/pregnancy, Accelerates metabolism of many other drugs, BCP, coumadin, digoxin, DM meds. VitD levels may drop (supplement)
(Tuberculosis Tx)
Strepomycin;
CSF penetration poor, Injections 5days/wk, Contraindicated in pregnancy.
(Tuberculosis Tx)
What are the toxic effects of Rifampin?
Cholestatic jaundice (rare), fever, thrombocytopenia & renal failure.
(Tuberculosis Tx)
What are the toxic effects of Strepomycin?
Renal tubular damage
Vestibular damage
Ototoxicity
(Tuberculosis Tx)
Prazinamide;
Used in combination w/other TB meds
Shortens course to 6mos
Not advisable >60y/o
Toxic effect-hyperuricemia
What is hyperuricemia?
An excessive amount of uric acid in the blood.
(Tuberculosis Tx)
Ethambutol;
Deters resistance to bactericidal drugs
Toxic effects-optic nerve, inability to tell blue from green, impaired VA (both reversible early on if med is d/cd).
(Tuberculosis Tx)
What are the recommended drug combinations?
RMP & INH daily for 9mos or daily for 1mo & then twice weekly for 8mos (600mg RMP & 900mg INH)
RMP, INH, EMB & PZA for 2wk DOT, then RMP, INH, EMB & PZA 2X/wk for 6 mos.
(Tuberculosis Tx)
What are the CDC recommendations for drug combination therapy?
RMPH & INH qd for 6 mos w/PZA for the 1st 2 mos.
What is Pneumonia?
Acut infection of lung parenchyma including alveolar spaces & interstitial tissue.
What are the common microbes responsible for bacterial pneumonia?
S. pneumoniae (most common cause of community-acquired bacterial pneumonia.
H. influenzae
K. pneumoniae
What are the uncommon microbes responsible for bacterial pneumonia?
S. aureus
S. pyogenes
P. aeruginosa
N. meningitidis
Bacterial Pneumonia Etiology;
Usually acquired by bronchogenic spread of the pathogen, Suprainfection in pts previously infected by an upper or lower resp viral infection. Incidence of infection ↑w/age, most pts are >50 & have underlying COPD, cardiovascular or other chronic dz.
Streptococcus pheumoniae epidemiology;
Affects children & adults worldwide, Leading cause of illness in young peds, Causes illness & death among the elderly & pts w/underlying med conditions, 40,000 deaths annually in US, 1/2 could be prevented through use of vaccine, Fatality rate is 15-20% among adults.
Where does Streptococcus pheumoniae colonize?
Organism colonizes the upper resp tract
What types of illness can Streptococcus pheumoniae cause?
Disseminated invasive infections including; bacteremia & meningitis, Pneumonia & other lower resp tract infections, Upper resp tract infections including; otitis media & sinusitis.
Each year in the US, pneumococcal dz accounts for;
3,000 cases of meningitis
50,000 cases of bacteremia
500,000 cases of pneumonia
7 million cases of OM
Severe pneumococcal infections result from;
Dissemination of bacteria to the bloodstream & the CNS.
Define
disseminated;
Scattered or distributed over a considerable area, esp. applied to disease organisms; scattered throughout an organ or the body.
In adults what % of pneumococcal bacteremia is associated w/pneumonia?
60-87%
What are the risks for acquiring bacteremia amoung the racial groups?
Lower in whites than other races.
Black adulet 3-5 X higher than whites.
Invasive pneumococcal dz are exceptionally high among Alaskan natives, & Native Americans.
In what pts are H influenzae & K pneumoniae more commonly seen in?
COPD
Alcoholics
Elderly
What manifestations are common in a pt w/H influenza Bacterial Pneumonia?
Pleural effusion, Bacteremia, & other infections such as; Otitis, Sinusitis, Meningitis, Epiglottis, & Facial infection.
What is Bacteremia?
Bacteria in the blood.
What pts are at risk for K. pneumoniae?
Alchol abusers
COPD
Neonates
What are the manifestations of K. pneumoniae?
(lg gram - rod w/capsule)
"Currant jelly" sputum
Bulging fissure
Lung necrosis
What pts are at risk for S. aureus pneumonia?
IV drug users
Elderly
Pts w/recent influenza virus infection
Pts w/cystic fibrosis
What are the mainifestions of S. aureus pneumonia?
(gram + cocci in clusters)
Pleuritic CP
Multiple thin walled abscesses (pneumatoceles)
Cardiac murmurs
What other infections should be checked for in a pt w/S. aureus pneumonia?
Endocarditis
Abscesses
Skin furuncles
(from desemination)
Most common is bacteremia.
What pts are most at risk for P. aeruginosa Pneumonia?
Pts w/cystic fibrosis
Severly compromised resp defenses
Pts on respirators (P. aeruginosa usual cause)
What are the manifestations of P.Aeruginosa Pneumonia?
Gram - rod (encapsulated in pts w/cystic fibrosis)
Green sputum, fulminant course, Necrotizing w/multiple sm & lg abscesses.
Define fulminant;
Having a rapid and severe onset.
In a pt w/P. aeruginosa pneumonia what other infections should you look for?
Skin lesions ecthyma gangrenosum.
What bacterial cause of pneumonia is not very common now due to ABX used to tx URI?
S. pyogenes pneumonia
What bacterial cause of pneumonia is occasionally seen in epidemics in military recruits?
N. meningitidis
What bacterial pneumonia is due to environmental exposure to a infected rat population?
Y. pestis
What bacterial pneumonia is due to exposure w/contaminated soil in southeast asia?
B. pseudomallei
What are the S/Sx of bacterial pneumonia?
Malaise, high fever, dyspnea, chest discomfort, pleuritic pain, chest splinting, cough productive of purulent or blood-tinged sputum, tachypnea, tachycardia, cyanosis, confusion.
What chest sounds would you expect to hear in a pt w/early onset of bacterial pneumonia?
fine crepitant rales over the involved portion of the lung(s).
What chest sounds result from lobar consolidation (a sx of bacterial pneumonia)?
Dullness to percussion, vocal fremitus, whispered pectoriloquy, bronchial breathing.
Bacterial Pneumonia PE;
Lobar consolidation
Pleural effusions (pleural friction rub, dullness to percussion, ↓Breath sounds) Egophony, Lower lobe involvement may cause referred pain to abdominal area d/t diaphragmatic inflammation.
What is Egophony?
An abnormal change in tone, somewhat like the bleat of a goat, heard in auscultation of the chest when the subject speaks normally.
What is the most useful lab test for the initial dx of bacterial pneumonia?
Gram stain examinatio of sputum.
(Bacterial pneumonia)
Why can culturing sputum be misleading?
Because normal oropharyngeal flora may contaminate specimen during passage through the upper airways.
(Bacterial pneumonia)
Where should specimens be taken from?
Normally sterile sites; Blood cultures in septic pts, Pleural fluid from empyema, Special culture techniques, special stains serologic assays.
(Bacterial pneumonia)
Lung biopsies to identify?
Mycobacteria (may be TB), Mycoplasmas, Anaerobic bacteria, Chlamydiae, Viruses.
What is the classic radiologic feature of bacterial pneumonia?
Dense lobar consolidation, consolidations may involve one or more lobes, unilateral or bilateral. A pleural effusion may exist.
(Bacterial Pneumonia)
What X-ray findings would you expect for Klebsiella pneumoniae infection?
"Bulging fissure" sign, Upper lobar consolidation w/a bowing fissure.
(Bacterial Pneumonia)
What X-ray findings would you expect for Staphylococcus aureus infection?
Multiple bilateral nodular inflitrates w/central cavitation. In whildren one can seel ill-defined, thin walled cavities ("pneumatoceles), bronchopleural fistulas, & empyema.
(Bacterial Pneumonia)
What X-ray findings would you expect for Pseudomonas aeruginosa infection?
microabscesses which may coalesce into large abscesses.
(Bacterial Pneumonia)
If you see lung necrosis on a X-ray what microbes would you suspect?
Gram-negative rod infections;
Klebsiella
Proteus
E. coli.
Bacterial Pneumonia D/Dx;
Viral pneumonia, Atypical Pneumonia (Coxie), TB, Influenza, Lung CA.
Bacterial Pneumonia Management & Tx;
Resp support, O2, ABX, Hospitalization, Antipyretics, Hydration.
How are ABX selected for Bacterial Pneumonia?
Gram stain results, If gram stain is not performed or does not establish a dx, ABX are selected on the basis of probabilities according to pts age, epidemiology, host risk factors & severity of illness.
Which baterias can cause Atypical Pneumonia?
Mycoplasma pneumoniae (most common), Legionella sp (Legionnaire's dz), Francisella Tularesis (Tularemia), Bacillus anthracis (anthrax), Bortadella pertussis (Whooping cough), Chlamydia psittaci (psittacosis), Chlamydia trachomatis, Chlamydia pneumoniae, Coxiella burnetii, Q fever.
Which viruses can cause Atypical Pneumonia?
Influenza
Parainfluenza *
Respiratory syncytial virus *
Adenovirus
Which fungi can cause Atypical Pneumonia?
Histoplasma capsulatum (histoplasmosis)
Coccidioides immitis (occidiodomycosis)
Pneumocystis carinii/jiroveci (Pneumocystosis)*
Aspergillus fumigatus (Aspergillosis)*
Which atypical pneumonia ranks second only to S. pneumoniae among all pneumonias due to infectious dx?
Mycoplasma pneumonia, cause of pneumonia in 20-25% of all age groups & to persist in certain persons for weeks to mos, resulting in prolonged reduced pulmonary clearance & airway hyper-responsiveness.
Mycoplasma pneumonia etioloby;
Aka; Atypical, Walking or Eaton agent pneumonia. Outbreaks occur year round. Tends to >in adolescents & young adults, Males > Females. Transmission person to person.
What is the incubation period of Mycoplasma pneumonia?
10-21 days
Mycoplasma pneumonia pathophysiology;
Destroys ciliated epithelial cells of the respiratory tract mucosa, causes interstitial pneumonitis, bronchitis & bronchiolitis. Peribronchial areas are infiltrated w/plasma cells & sm lymphocytes, w/in the bronchial lumina are neutrophils, macrophages, fibrin strands & epithelial cell debris.
What are the initial S/Sx of Mycoplasma pneumonia?
Resemble influenza; Malaise, Sore throat, Dry cough ↑ in severity as the dz progresses, productive sputum that is mucoid, mucopurulent or blood-streaked.
How does Mycoplasma pneumonia progress?
Gradually
How long does Mycoplasma Pneumonia usually last?
Acute symptoms for 1-2wk followed by gradual recovery, pts may continue to have symptoms w/fatigue & malise for several wks, spontaneous recovery is the rule.
What can what can severe Mycoplasma Pneumonia develop into?
Adult Respiratory Distress Syndrome
Pts who have Mycoplasma Pneumonia can have what derm sx?
Maculopapular rashes (10-20%)
Erythema Multiform
Stevens-Johnson Syndrome
Mycoplasma Pneumonia PE;
PE tends to be unimpressive in contrast w/the pts complaints & X-ray changes.
Mycoplasma Pneumonia Lab findings;
Gram stain of sputum shows; sparse bacteria, mixture of PMNs & mononuclear cells, & clumps of desquamated resp epithelial cells. WBC ct is normal-modestly elevated.
Mycoplasma Pneumonia Culture;
Difficult to culture & requires 7-21 days to grow; successful in 40-90% of cases.
Mycoplasma Pneumonia Cold Agglutinin;
Is considered + if there is a fourfold ↑ in titer w/sequential specimens or a single tieter >=1:64
What is the most practical method of confirming a Mycoplasma Pneumonia dx?
The use of serologic assays. Most often, a single elevated IgM or a fourfold rise in titer w/a peak titer >=1:64 at 2 to 4 wk p the onset of sx.
What other labs can be ran to dx Mycoplasma Pneumonia?
Complement fixation test, IgM by latex agglutination or ELISA, Cold agglutinins***, Indirect Flourescent Antibody test to detect Mycoplasma Pneumonia antibodies.
Mycoplasma Pneumonia D/Dx;
Chlamydia pneumonia, Legionella pneumonia, Chlamydia psittaci, Chlamydia trachomatis, Coxiella burnetii (Q fever)
Mycoplasma Pneumonia Tx;
Most pt's recover w/out tx, Mycoplasmas do not respond to ABX that interfere w/cell wall structure (including beta-lactam ABX), Meds of choice tetracycline or erythromycin (A 500mg q6h, P<8yr 30-50mg/kg/day)
Chlamydia pneumonia causes what % of community acquired pneumonia?
10%
Chlamydia pneumonia Etiology;
C. pneumoniae
C. trachomatis
C. psittaci
Chlamydia pneumonia S/Sx;
Pharyngitis, Bronchitis, Pneumonitis, Persistent cough, fever, sputum production (but are not seriously ill), S/Sx resemble M. Pneumonia, primarily in older children & young adults.
Chlamydia Trachomatis is a common cause of pneumonia in?
Infants aged 3-8wk.
Chlamydia Pneumoniae is distinguishable from psittacosis & not epidemiologically linked w/?
Birds
What is Chlamydia Psittacosis?
An infectious atypical pneumonia caused by Chlamydia Psittaci & transmitted to humans by certain birds.
Which birds transmit Chlamydia Psittacosis?
Parrots, Parakeets, Lovebirds, Poultry, Pigeons, Canaries, Snowy egrets, Herring gulls, Petrels, Fumars
Chlamydia Psittacosis etiology;
Usually caused by inhaling dust from feathers or excreta of infected birds, or by the bite of a infected bire, sometimes by inhaling cough droplets of infected pts or venereally, Human to Human transmission is associated w/highly virulent avian strains.
Define venereal;
Pert. to or resulting from sexual intercourse.
How long is the incubation period for Chlamydia Psittacosis?
1-3 weeks
Chlamydia Psittacosis S/Sx;
Onset insidious or abrupt, temperature gradually rises, chills, malaise, anorexia, cough develops (initally dry but at times mucopurulent), Pneumonia & frank consolidation may occur w/2ndary purulent lung infection, temp is elevated for 2-3wks then falls slowly.
What determines the severiry of Chlamydia Psittacosis Pneumonia?
Pt's age & extent of the pneumonia.
Chlamydia Psittacosis prognisis;
A progressive, pronounced increase in pulse & resp rate is a ominous sign, Mortality may reach 30% in severe untx cases, (higher rates are reported w/virulent strains) A gradual convalescence may be prolonged, especially in severe cases.
Chlamydia Psittacosis D/Dx;
Influenza, Typhoid fever, Mycoplasmal pneumonia, Legionnaires' dz, Q fever.
Chlamydia Psittacosis Tx;
Avoid infected sick birds, especially dust from feathers & cage contents, Tetracycline 1-2g/day po in divided doses q6hr or doxycycline 100mg bid (tx for at least 10days), Strict bed rest, O2 when needed, & cough control.
What is Legionnaires' Dz?
>30 species, 19 have been implicated as caustice agents of pneumonia.
These organisms are morphologically dimilar, share biochemical characteristics & cause simular dzs.
Name some of the species of Legionnaires' that cause Legionnaires' Pneumonia?
Legionnaires' pneumophila (most causative agent)
Legionnaires' micdadei (most causative cause)
L. bozemanii & L. dumoffi
What is the spectrum of Legionnaires' dz?
Asymptomatic seroconversion, A self-limited, flu-like illness w/out pneumonia, "pontiac fever", Pneumonia, Rare localized soft tissue infections.
Legionnaires' Dz risk factors;
Occur at any age,> in middle aged men, Smoking, EOTH abuse, Immunosuppression, especially corticosteroids,
Legionnaires' Dz epidemology;
1-8% of community acquired pneumonias resulting in hospitalization, 4% of lethal nosocomial pneumonias. Occurs sporadically, predilection for late summer & early fall. Person-to-person transmission has not benn demonstrated. Outbreaks tend to occur in hospitals & hotels. w/contaminated H2O supply, organisms spread from evaporative condensers of air conditioning systems or contaminated showerheads.
What is the incubation period of Legionnaire's Dz?
2-10 days
Legionnaire's Dz S/Sx
Prodromal phase;
Malaise, Fever, H/A, Myalgias
Define Prodromal;
Pert. to the initial stage of a disease; the interval between the earliest symptoms and the appearance of a rash or fever.
Define Myalgia;
Tenderness or pain in the muscles; muscular rheumatism.
Legionnaire's Dz S/Sx;
Initial cough nonproductive w/subsequent production of mucoid sputum, High fever.
Sometimes; bradycardia, Diarrhea, Altered mental status.
Legionnaires' Dz Lab findings;
Leukocytosis; WBC 10,000-15,000/ul, CSF studies are normal, Stool is neg for blood & WBCs
Legionella sp. is stained w/Dieterle silver stain & direct fluorescent antibody staining, Urine test for Legionella antigen, Culture.
Legionnaire's Dz CXR findings;
Unilateral, patchy segmental or lobar slveolar infiltrate(Early on), (later in dz) many pts develop bilateral involvement & pleural effusions, occasionally lung abscesses & multiple rounded densities suggesting septic emboli.
Legionnaire's Dz Tx;
Erythromycin (drug of choice) 1g IV q 6hr, less severe 500mg po qid, Seriously ill erythromycin w/rifampin 300mg bid po or IV, Tx should be for >=3wk.
Cipro 750mg po bid
Azithromycin 500mg (initial dose) 250mg qd
Which viruses can cause Atypical pneumonia?
Resp Syncytial, Parainfluenzsa, Influenza A & B, Cytomegalovirus (CMV), Adenovirus, Varicella-Zoster, Epstein-Barr, Coxsackie, Hanta.
Atypical pneumonia Viruses Eitology;
Viruses invade the bronchiolar epitheliam, causing bronchiolitis, infection extends to the pulmonary interstitium & alveoli, causing pneumonia.
How do the affected areas respond to viral atypical pneumonia?
Congested, +/-hemorrhagic, Display inflammatory reaction composed of mononuclear cells.
With viral atypical pneumonia what do the alveoli contain?
Fibrin, mononuclear cells, +/-neutophils, +/-hyaline membranes.
In viral atypical pneumonia what viral inclusions may occur?
Adenovirus, CMV, Respiratory syncytial virus, Varicella-zoster.
Viral atypical pneumonia S/Sx;
H/A, Fever, Myalgia, Cough(produces scant sputum).
Viral atypical pneumonia lab findings;
Sparse bacteria & a dominance of monocytes on smears of sputum, +throat washings or tissue, ID of typical inclusions in cytopathology or biopsy speciments, serologyic assays, viral culture (if available)
Viral atypical pneumonia X-ray findings;
(most common) Interstitial pneumonia or peribronchial thickening. Lobar consolidation & pleural effusions are not common but may occur w/bacterial superinfection.
Viral atypical pneumonia Tx;
Acyclovir 5-10mg/kg q 8hr (adults) or 250-500mg/m2 BSA q 8hr (peds)
CMV pneumonia may be tx w/ganciclovir 5mg/kg IV bid & immune globulin (IV immune globulin or CMV immune globulin)
Viral atypical pneumonia complications;
Superimposed bacterial infections by: Streptococcus pneumoniae, Staphylococcus aureus, HiB, Group A hemolytic streptococci, Neisseria meningitidis.
(Atypical Pneumonias Fungal)
Histoplasmosis Definition;
Dz caused by histoplasma capsulatum, causing primary pulmonary lesions & hematogenous dissemination.
(Atypical Pneumonias Fungal)
Histoplasmosis Risk factors;
(Severe dz more common p heavy, prolonged exposure)
Men
Infants
Compromised T-cell-mediated immunity.
(Atypical Pneumonias Fungal)
What are the endemic areas of Histoplasmosis?
Ohio-Missippi river valleys extending into parts of northern Maryland, Southern Pennsylvania, Central New York, California & Texas
(Atypical Pneumonias Fungal)
Histoplasmosis Patho;
H. capsulatum grows in soil & material contaminated w/bat or bird droppings, spores become airborne when contaminated soil is disturbed, breathing the spores causes the infection. The dz is not transmitted person to person.
(Atypical Pneumonias Fungal)
Acute primary Histoplasmosis S/Sx;
Usually asymptomatic.
Sometimes; Non specific sx, Fever, Cough, Malaise of varying severity, Acute pneumonia (sometimes evident on PE or CXR)
(Atypical Pneumonias Fungal)
Progressive Disseminated Histoplasmosis S/Sx;
Hematogenous Spread from the lungs (what isn't controlled by normal cell-mediated host defense mechanisms); Hepatosplenomegaly, Lymphadenopathy, Bone marrow involvement, Oral or GI ulcers. Severe manifestations occur in infants & immunocompromised pts.
(Atypical Pneumonias Fungal)
Progressive Disseminated Histoplasmosis in AIDS pts;
One of the defining opportunistic infections. AIDS pts may develop severe acute pneumonia w/hypoxia suggestive of Pneumocystis carinii infection & hypotension, mental status changes, coagulopathy or rhabdomyolysis.
(Atypical Pneumonias Fungal)
Chronic cavitary histoplasmosis S/Sx;
Atypical pulmonary lesions (resemble cavitary TB), worsening manifestations cough & dyspnea, progresses to disabling resp dysfunction. Dissemination does not occur.
(Atypical Pneumonias Fungal)
Histoplasmosis Labs Smears & Cultures Findings;
Tissue specimens;
characteristic clusters of small, oval yeast cells w/in macrophages, blood monocytes or neutrophils. Intracellular yeasts may be seen in Wright's or Giemsa.
(Atypical Pneumonias Fungal)
Histoplasmosis Serology Testing Culture;
Sputum, lymph nodes, bone marrow, liver biopsy, blood, urine.
(Atypical Pneumonias Fungal)
Histoplasmosis Serology Testing Findings;
Antigen can be detected in serum, urine, CSF or bronchoalveolar lavage samples by enzymatic assay or radioimmunoassay.
(Atypical Pneumonias Fungal)
Acute primary Histoplasmosis Tx;
Usually self-limited (rare fatalities p massive infections have been reported)
(Atypical Pneumonias Fungal)
Progressive Disseminated Histoplasmosis Tx;
Itraconozole for less severe cases.
Amphotericin B (IV) for more severe disseminated cases.
(Atypical Pneumonias Fungal)
Progressive Disseminated prognosis;
(untx) has a fatality rate >90%
(Atypical Pneumonias Fungal)
Chronic cavitary histoplasmosis prognosis;
Can cause death from severe resp insufficiency.
Define Coccidioides immitis;
Dz caused by fungus C. immitis, usually occurs as a acute benign asymptomatic or self-limited resp inf, occasionally disseminating to cause focal lesions in skin, subQ tissues, lymph nodes, bones, liver, kidneys, meninges, brain or other tissues.
Where is Coccidioidomycosis endemic?
Southwestern USA; Including the central valley of California
How are Coccidioidomycosis infections aquired?
Inhalation of spore-laden dust.
Coccidioidomycosis Patho;
C. immitis conidia (spores) convert at 98.6 degrees to form lg tissue-invasive spherules, they rupture, each releases multiple sm endospores that may form new spherules.
Primary Coccidioidomycosis Eitology;
Usually asymptomatic, but nonspecific resp sx resembling influenza or acute bronchitis sometimes occur, less often acute pneumonia or pleural effusion.
Primary Coccidioidomycosis S/Sx;
Fever, Cough, CP, Chills, Sputum production, Sore throat, Hemoptysis, Scattered rales w/or w/out areas of dullness to percussion over lung fields. Usually leukocytosis & sometimes eosinophillia.
Progressive Coccidioidomycosis S/Sx;
Low grade fever, anorexia, wt loss, weakness. Extensive pulmonary envolvement may cause progressive cyanosis, dyspnea, & discharge of mucopurulent or bloody sputum. Extrapulmonary lesions are usually focal, involving one or more tissue sites in bones, joints, skin, subQ tissues, viscera, brain or meninges
Progressive Coccidioidomycosis Eitology;
May develop in weeks to years after primary infection. Men > Women.
What labs should be ordered for a pt with Coccidioidomycosis?
Complement fixation for IgG anticoccidioidal antibodies (most useful test) Titers >/= 1:4 in serum are consistant w/current or recent infection. Higher tiers >/=1:32 signify an increased likelihood of extrapulmonary dissemination.
Progressive Coccidioidomycosis Tx;
IV amphotericin B is preferable for severely ill pts. AIDS pts require maintence therapy to prevent relapse. Tx for meningeal coccidioidomycosis must be continued for mos to life long. Surgical removal of involved bone may be necessary. Untreated disseminated coccidiomycosis is usually fatal. Mortality of HIV pts exceeds 70% in 1st month of dx.
Tx for mild to moderate Coccidioidomycosis
=/> Fluconazole 400mg/day or Itraconazole 400mg/day.
What is Pneumocystosis?
P. Carinii in rats, P. jiroveci affects humans, Rare in immune competent pts, Occurs in 80% of AIDS pts w/high mortality.
Pneumocystosis Diagnostics;
DXR; diffuse interstitial pattern.
Can't culture; need organism to dx.
Pneumocystosis Tx;
Bactrim/Septra
What is Aspergillosis?
Clinical illness occurs w/tissue invasion or aberrant immunologic response (severe asthma excerbations) In immune compent pts causes chronic sinusitis. Invasive dz in HIV/AIDS pts, Necrotizing pneumonia w/dissemination of organism throughout body.
What is ARDS?
Adult respiratory distress syndrome, resp failure caused by various acute pulm injuries & characterized by noncardiogenic pulmonary edema, resp distress, & hypoxemia.
Adult respiratory distress Etiology;
Always caused by something else, Occurance >30% w/sepsis. Plasma & blood leak into interstitial & intra-alveolar spaces; atelectasis, inflammation in 2-3days, severe interstitial fibrosis 2-3wks, → stiff lungs, ↓ functional capacity (lungs to full of stuff), V/Q mismatch, hypoxemia, pulm HTN.
Adult respiratory distress S/Sx;
Dyspnea progressing to resp failure, lung sounds; normal>rales>wheezes, hypoxemia that doesn't resolve w/O2 (incl intubation w/100% FI02)
Adult respiratory distress D/Dx;
Heart failure
PE
PCP
Adult respiratory distress Tx;
O2 therapy (inc vent), TPN, hydration, swan ganz, ABGs, tx underlying cause, inhaled nitric oxide, suppress tumor necrosing factor (TNF) w/ketoconazole, aerosolized surfactant.
Adult respiratory distress Labs;
ABG; acute resp alkalosis, low PO2, norm or low PCO2.
Adult respiratory distress CXR;
Diffuse bilateral alveolar infiltrates, cardiac silhouette normal.
What is asthma?
Pulmonary dz characterized by; reversivle airway obstruction, airway inflammation, ↑ airway responsiveness to a variety of stimuli.
What is the leading cause of hospitalization for peds?
Asthma
Asthma Patho;
Bronchospasm, Hyper-responsive/Hyper-reactive airways, Inflammatory mediators, cholinergic reflex bronchoconstrictions.
Asthma Bronchoconstricion Patho;
Smooth muscle contracion, used to be the only patho acknowledged tx in asthma.
Asthma Hyperresponsiveness Patho;
Exaggerated bronchoconstrictior response to different stimuli, degree of hyperresponsiveness is linked to the extent of inflammation, cause unknown, struction changes in airways may contribute.
Asthma What results from desquamation of epithelium;
loss of relaxing factor & of prostaglandin E2 (both reduce contractile response to mediators.
Asthma What is the result from epithelium damage;
Decreased 'Neutral Endopeptidases', these are normally responsibe for metabolizing bronchchoconstricting mediators, Airway remodeling causes slightly thicker airways.
In Asthma what are released &/or formed as a consequence of allergic reaction in the lungs?
Inflammatory mediators; Histamines & Products of arachidonic acid metabolism transietly increase airway hyperresponsiveness (leukotrienes (LTC4 & LTD$ & Thromboxane)
In Asthma what inflammatory mediators are the key activatiors?
T-cell, they produce cytokines, perpetuate airway inflammation (Interleukin (IL4) is necessary for IgE production & Interleukin (IL5) attracts eosinophils) T-cells promote growth, differentiation, activation & migration of inflammatory cells to airways.
In Asthma what is cholinergic reflex bronchoconstriction?
Response to inhalation of irritant. Neuropeptides cause; Vascular permeability, Mucus secretion, Bronchoconstriction, Bronchial vasodilation (Neuokinin A, Calcitonin peptide) → obstrucion & ventilation that is not uniform (V/Q mismatch)
Asthma Acute attack S/Sx;
Tachypnea, Tachycardia, Sit upright, lean forward, accessory muscle use, anxious, Prolonged expiratory phase w/high pitched wheezes, hyperinflated chest, choarse rhonchi, fatigue, cyanosis, confusion, quiet chest.
What are the life threatening signs in a Acute attack of asthma?
Dyspnea at rest, inability to speak, cyanosis, pulus paradoxus (9.20-30mmHg), use of accessory muscles.
Asthma labs;
ABG; pH, blood gasses.
Eosinophil ct; >250-400 present regardless of allergic factors involvement in attack.
Sputum; Tenacious, Rubbery, Whitish, Charcot-Leyden crystal present, PMN & bacteria rarely present.
Asthma PFT;
Useless during acute attack, degree of airway obstruction, measure response to inhaled allergens & chemicals, before & p bronchodilatior, Static lung capacities, Dynamic lung capacities.
Asthma CXR;
Vary depending on severity of dx;
Hyperinflation
Atelectasis
Asthma Dx;
Consider anyone who wheezes, persistent cough, catagorize severity to direct tx.
Asthma D/Dx;
Foreign body, URI, Epiglottitis, RSV, COPD, CHF, other bronchial obstructions.
Asthma Rx What is a Agonist?
Adrenergic drugs, relax bronchial smooth muscle & modulate mediator release;
Epinephrine & selective Beta 2 agonists.
Asthma Rx Beta 2 agonist for acute attack?
Albuerol, Proventil, Ventolin, Maxair (Pirbuterol), Xopenex (Levabuterol) active for 6-8hrs. (some cardiac adverse R);P inhalation rapid onset in mins, active for 4-6h
Asthma Rx Beta 2 agonist for maintence;
Salmetorol or Foradil; long-acting (↑12hrs) Helps control nocturnal sx, combined w/a inhaled corticosteroid is Advair.
Asthma Rx Methylxanthine;
Theophylline; relaxes bronchial smooth muscle & has some modest anti-inflammatory activity, ↓ microvascular leakage into the airway mucosa, inhibit late allergen response, ↓ infiltration of eosinophils into bronchial mucosa, ↓ T lymphocytes into epithelium, ↑ myocardial & diaphragmatic contractility, extended release useful for nocternal asthma, narrow therapeutic index,
Asthma Rx anticholinergic drugs;
Atrophine & ipratropium bromide; Inhibits muscarinic cholinergic receptors that cause airway obstruction, block reflex bronchoconstriction due to irritants or to reflux esophagitis.
Asthma Rx Corticosteroids;
Inhibit the attraction of inflammatory cells & inhibits their activation, Blocks leukotriene synthesis, inhibits cytokine production & adhesion protein activation, block the late response to allergens, w/long-term use, bronchial hyperresponsiveness gradually decreases, use systemic (5-7days) to kick start. Pts still need albuterol for acute attacks.
Asthma Rx Mast Cell stabilizers;
Cromolyn & nedocromil (Intal);(safest antiasthmatic meds)Inhalation prophylactically, inhibit mediator release from inflammatory cells. Reduce airway hyperresponsiveness, block early & late responses to allergens.
Asthma Rx Leukotriene modifiers;
Montelukast (Singular) & Zafirlukast (Accolate); Selective competitive inhibitors of LTD4 & LTE4 receptors & sileuton, a 5 lipoxygenase inhibitor.
What are the stages of asthma attacks?
I-Mild
II- Moderate
III-Severe
IV- Respiratory failure
What tx should be administered for a pt w/Asthma in Stage I?
Bronchodilatior Inhaler/Nebulizer, Albuterol (MR X3)
Epi (MR X1-2 in 20-30min)or Terbutaline SQ (<CV affects)
What tx should be administered for a pt w/Asthma in Stage II?
Stage I Tx + Corticosteroid 120-180mg po in 3 divided doses for 48 hr then ↓ dose, Peds 1mg/kg/day max 60mg.
ABGs
What tx should be administered for a pt w/Asthma in Stage III?
ABG immediately, albuterol neb sol 5mg/ml tx, (10-15mg/hr Adults, Peds 0.5mg/kg/h max 15mg/h) O2 tx. Methyleprednisolone IV, Admit if failure to improve, worsening fatigue, relapse p repeated agonist & aminophyilie tx, sig↓ in PaO2 or ↑ in PaCO2.
What tx should be administered for a pt w/Asthma in Stage IV?
Beta agonist, Theophyiline, Methyleprednisolone 1-2mg/kg IV q 4-6h,if no response to aggressive 2agonist & corticosteroid tx, & have fatigue & progressive deterioration in ABGs & Ph should be considered for intubation.
Why is sedative use in a non-intubated asthma pt dangerous?
It can knock out their resp drive.
Why is volume-cycled ventilation used in a Asthma pt?
If pt has resp acidosis it is a mechanical problem that must be relieved, VC ventilation can provide reasonably constant alveolar ventilation when airway resistance in high & changing.
What is Bronchiectasis?
Congenital or caquired disorder of the lg bronchi characterized by permanent abnormal dilation & edstruction of bronchial walls.
Bronchiectasis Etiology;
Recurrent inflammation or infection, Cystic fibrosis (causes 50% of all cases), TB, Fungal infections, Lung abscess, Pneumonia, Rheumatic dz, Congenital & acquired immunodeficiencies (drugs).
Bronchiectasis S/Sx;
Chronic cough, Production of copious purulent sputum, Hemoptysis, Recurrent pneumonia, Wt loss, Anemia, Crackeles @ bases, Clubbing, Copious foul smelling purulent sputum, Obstructive pulm dys w/hypoxemia, Crowded bronchial markings, cystic spaces @ bases, fibrosis.
Bronchiectasis Acute Exacerbation Tx;
ABX (amoxicillin or augmentin)
Daily chest physiotherpay w/posteral drainage.
Inhaled bronchodilators.
Bronchiectasis Prophylaxis;
Inhaled aminoglycosides (helps prevent infections)
Bronchiectasis Complications;
Hemoptysis (become anemic), Cor pulmonale, Amyloidosis, Veseral Abscess.
Bronchiectasis Dx;
Bronchoscopy
Srugical resection
What is chronic bronchitis?
Presence of a mucus-producing cough, most days of the month, 3 months a year, for 2 successive years w/out other underlying dz to explain the cough.
Chronic Bronchitis risk factors;
Females>males, >45yrs, Smokers, Sx worsen when air pollutants↑ (especially smokers), Occupational exposure to dust & irritating fumes.
Chronic bronchitis Etiology;
(pts are more at risk for infection) The lining of the bronchial tubes become inflamed, when the bronchi are inflamed &/or infected, less air is able to flow to & from the lungs & heavy mucus or phlegm is coughed up.
What is emphysema?
The breakdown of the walls of the alveoli. The damaged alveoli cannot exchange O2 & CO2, the bronchioles lose elasticity & collapse on exhalation, trapping air in the lungs, the trapped air keeps sufficient levels of O2 from entering the lungs.
What is COPD?
A general term used for chronic bronchitis, emphysema, & chronic asthma (most pts have chronic bronchitis & emphysema) COPD worsens gradually, causing limited airflow in & out of the lungs.
COPD Epidemiology;
Emphysema & chronic brochitis affect about 16milllion people in the US, close to 11% of the population.
COPD Risk factors;
#1 Smoking
Alpha1-antitrypsin (AAT) deficiency-deficiency of alpha1-protease inhibitor, Elastase (enzyme that breaks down elastin) is no inhibited resulting in elastin degradation (onset by middle age)
What is the most common sx of COPD?
Dyspnea, gradual onset 1st noticed during px exertion or during acute exerbations, pts >60, closely associated w/lung function decline & is not always associated w/decreaased O2 in the blood.
COPD S/Sx cough;
Begins as a AM cough & slowly progresses to an all-day cough, produces small amts of sputum, clear or whitish but may be discolored, sputum production ↓ when one quits smoking, the progression of the cough is very slow (any change in chronic cough should be throughly investigated)
COPD S/Sx hemoptysis;
Common cause of hemoptysis, usually during acute exacerbation, w/productive cough w/purulent sputum (may be a sign of Lung CA)
COPD S/Sx Pink Puffer;
Emphysema type predominate; Airflow out is limited & exhalation takes longer, alveoli lose elasticity, pt forcefull exhales, ↑ calorie burn for breathing, pts are SOB & it is harder to eat.
COPD S/Sx Blue bloater;
Chronic bronchitis predominate type; Poor O2 supply pt appears cyanotic, PE reveals a bluish tinge to skin, lips & nail beds.
COPD S/Sx Barrel Chest;
Chest wall is enlarged, accessory breathing muscles become less efficient (contributes to SOB), When lungs become enlarged, the diaphragm is displaced downward & is unable to contract efficiently, dyspnea occurs when arms are raised, tripod position.
COPD S/Sx Lower extremity edema;
Pulmonary artery pressures ↑, Right ventricular failure, which leads to lower extremity edema.
COPD labs;
EKG Check hrt function & R/O hrt dz, HXR for lung changes, PFT for lung volume & air flow, Pulse ox for O2 sat, ABGs check amt of O2 & CO2 in blood, Exercise test to check O2 level w/exertion.
COPD EKG;
Cor pulmonale, R wave lg or lger than S wave in V1, Right axis deviation >110 degree w/out RT bundle branch block.
COPD X-RAY;
Low flat diaphragn in frontal view (overdistenion of lungs), In lateral view, wedening of the retrosternal sirspace & ↑ in angle formed by the sternum & diaphragm form acute to >=90degree. Hrt shadow is long & narrow, lungs are hyperlucent.
COPD Emphysema X-Ray;
Bullae >1cm
COPD Lab sputum;
In stable chronic bronchitis is mucoid, During exacerbation, purulent w/influx of neutrophils gram stain may show; Strep Pneumoniae, HiB, Moraxella catarrhalis, Gram neg rods, staphylococcus.
COPD PFT;
The FEV1 & FEV1/FVC fall progressively as severity ↑, FEV1 is less variable & can be predicted more accurately from age, sex & ht.
(COPD PFT) Can PFT distinguish between chronic bronitis & emphysema?
No
COPD Arterial blood gases;
ABGs measurements detect hypoxemia & hypercapnia & determine their severity(During early stages they are mild), As dz progresses, hypoxemia becomes more severe & hypercapnia predominates. Hypercapnia occurs as the FEV1 falls below 1L. Abnormalties worsen during acute exacergations & excerise & sleep. Functional residual capacity & residual volume are ↑, vital capacity is ↓.
COPD D/Dx;
TB & CA
COPD TX;
Fluvax annually, Pneumovax, Smoking cessation, Bronchodialtor drugs, Anticholinergic drugs, Theophylline, Corticosteroids, ABX prn, Good hydration (thin secretions), O2 tx, Energy conservation for ADLs, Nutrition ED, Lung transplant, Lunvolume reduction surg, Pulm rehab programs, Tx of alpha-antitrypsin deficiency w/purified human 1-antitrypsin (very expensive)
What is a pleural effusion?
Abnormal accumulation of fluid in the pleural space.