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-12- Asthma and COPD

September-17-08 9:26 AM

Notes By:

Obstructive lung disease

* Asthma is a chronic inflammatory syndrome, not one disease, that is characterized by increased responsiveness of tracheobronchial tree to a multiplicity of stimuli. * Comprised of multiple disorders with common symptoms with distinct and probably different pathogenetic mechanisms * Leads to reversible obstruction of bronchial tree Epidemiology * Asthma * most common chronic disease of childhood. * Male: female ratio: * 2:1 - childhood * 1:1 - adulthood * 4-5% population of US is affected * Prevalence is increasing. Etiological Classification * Extrinsic Asthma (allergic or atopic asthma) * Intrinsic Asthma (nonatopic asthma) * Mixed group Extrinsic vs. Intrinsic Is it real??? * This nomenclature is falling out of use because it lacks discriminative power in making diagnosis of disease or defining treatment strategies Etiology * Intrinsic Asthma: * Extrinsic Asthma: * Irritant exposure: * Indoor allergens * Air pollution, tobacco smoke, fumes, perfumes, household cleaning agents, * House dust mites (most common), animal insecticides, fresh paint, and cold air proteins, mold spores, and cockroaches * Infection: * Outdoor allergens * Upper respiratory infection * Pollens and mold spores * Gastroesophageal reflux * Exercise * Emotional stress You can see what the stimuli are. Intrinsic, most common * Pharmacological agents Beta blockers, NSAIDS is the house dust mite. Etiological Classification. Not going to test on, just for education. Risk Factors * Family History * 1 parent w/ asthma: up to 25% risk * 2 parents w/ asthma: up to 50% risk * Parental smoking * Aspirin or NSAID allergy * Infections * Strenuous exercise in high pollution areas * Occupational exposure Some of the cells that are involved Asthma - Pathogenesis * There is a state of persistent subacute inflammation of airway * Early phase asthma reaction: * Bronchospasm caused by: * Antigen stimulation of bronchial wall * Mast cell degranulation * Late phase asthma reaction: * Bronchial inflammation due to: * Inflammatory cells recruitment * Inflammatory mediators release Cellular sources of Inflammatory mediators Asthma Pathogenesis * TH2 cells, B cells, mast cells, eosinophils, epithelial cells and other inflammatory cells play important role in pathogenesis of Asthma a. Pharmacological stimuli for asthma i. Aspirin (some other NSAIDS), B-blockers, coloring agents (tartrazine), and sulfiting agents (metabisulfite and sulfur dioxide) ii. About 10% patients with asthma have aspirin sensitivity iii. Acetaminophen and sodium salicylate are better tolerated iv. Aspirin likely causes chronic over-excitation of cysteinyl leukotrienes which in turn activates mast cells b. Environmental pollution and occupational factors i. Air pollutants like Ozone, nitrogen dioxide, sulfur dioxide increase frequency of attacks in asthmatics ii. Wood, vegetable dust, insect dust, biological enzymes, serums and secretions, animal proteins like oyster, crabs, prawns, bees, moths etc. iii. Industrial chemicals and plastics c. Infections exacerbating asthma i. Respiratory infections (especially viral infections) are most common stimuli that exacerbate asthma ii. In young children - RSV and parainfluenza virus iii. In older children and adults- rhino virus and influenza virus iv. Likely mechanism is production of T-Cell derived cytokines d. Exercise precipitating asthma i. Exercise is a common precipitant of acute asthma ii. Attacks typically follow exertion iii. Severity depends on levels of ventilation during exercise (more in running then in walking) and temperature and humidity of air (more in dry cold air) iv. Likely mechanism is hyperemia and capillary leakage in airway wall e. Emotional stress precipitating asthma i. Emotional stress can precipitate asthma likely through vagus mediated changes in airway calibers and through endorphins Clinical Features Wheezing Triad * Cough with or w/o sputum production Episodic dyspnea, often aggravated by exercise * Chest pain or Tightness in the chest * Use of accessory respiratory muscles - Nasal flaring and Intercostal retractions * Exhalation more than twice as long as inspiration Clinical Features * Emergency symptoms: * Extreme difficulty in breathing If you have someone who is dyspneic and is not wheezing, then they have a really bad sign.

Common sense stuff.

We get a persistent subacute inflammation. These are some

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* Extreme difficulty in breathing * Pulsus paradoxus - Pulsus paradoxus is an inspiratory reduction in systolic pressure >10 mmHg. This occurs due to reduced left ventricle stroke volume during inspiration, which worsens during acute asthma * Cyanosis of the lips and face * Decreased level of consciousness * Severe anxiety * Tachycardia * Sweating * Difficulty in talking Differential diagnosis -Asthma * Upper airway obstruction by tumor, laryngeal edema stridor is more prominent * Endobronchial obstruction - Foreign body aspiration, neoplasm - Persistent localized wheeze with paroxysms of cough * Left ventricular failure basilar rales, gallop rhythm, LE edema * Chronic bronchitis No symptom free period * Recurrent pulmonary emboli pulmonary angiography, spiral CT Investigations * Pulmonary Function Tests (PFT): * Obstructive pattern: * Decreased in FEV1 (forced expiratory volume in one second) * Decreased or normal FVC (functional vital capacity) * Decreased FEV1/FVC * An improvement of > 15% in FEV1 with beta agonists is diagnostic. * Metacholine or histamine challenge test: * Indicated when spirometry is normal. * Causes bronchoconstriction * Exercise stress test: * Useful in documenting exercise-induced asthma. * Evaluating severity of asthma with PFT: * Mild asthma: PEF or FEV1 80% * Moderate asthma - PEF or FEV1 61 - 79% * Severe asthma: * PEF or FEV1 60% * Arterial blood gas (ABG): * Indications: * Severely symptomatic * FEV1 < 30% after initial therapy * PaO2 < 60 is a sign of severe hypoxia * PaCO2 is initially low, but later becomes high. * An increased PaCO2 (>45) is a sign of impending respiratory failure and may requires hospitalization For the boards, not for him! * Pulse oximetry: Monitors oxygen saturation * CBC: Blood eosinophilia greater than 4% or 300-400/mL supports the diagnosis of asthma * IgE: Total serum immunoglobulin E levels greater than 100 IU may occur in allergic asthma * Sputum exam: Shows eosinophils and Curschmanns spirals, Charcot-Leyden crystals, Creola bodies Chest x-ray: * Usually normal or may show hyperinflation * Indicated to rule of pneumonia, CHF, pneumothorax Sinus films: * Sinusitis may precipitate attacks. * CT scan may show bronchial thickening (not routinely done) PA and lateral film. Look how inflated this is, Increased AP diameter. In general, this should not be more than half of that (that = chest cavity) Treatment * Desensitize for allergens if allergens have been identified * Drug categories: * Bronchodilators: * Beta-adrenergic agonists * Anticholinergics * Methylxanthine * Anti-inflammatory agents: * Corticosteroids * Mast cell stabilizers * Leukotriene antagonists

What are a couple of other conditions with pulsus paradoxicus? Cardiac tamponade. Restrictive pericarditis. These people get really scared, like with PE, when they have a bad attack they know something is happening. They get tachycardic. If they cant tell you whts going on, then thats another really bad sign because they are too out of breath.

If you have a toddler with unilateral wheezing, then its aspiration of foreign body. You just do bronchoscopy and remove it. Cancer can cause wheezing. In congestive heart failure, its not uncommon. In CHF you can have wheezing. You can have it in chronic bronchitis and with recurrent Pes.

PFTs are the gold standard. We havea decrease in the FEV1. If they havea nrmal test, we do a methylcholine challenge, which causes a bronchospasm, and then we reverse it. This is a slide to remember!

Professor has seen people with an FEV of less than 20%

ABGs will depend on where they are at. What is the first thing it will show, a respiratory alkalosis. They will be hyperventilating, then you will have an acidosis as they are tired. Chronic asthmatics keep logs of their peak flows. They have their own meters Would want to look at the sputum, but it may or may not help you.

We will always get a chest xray. We might do a CT scan, but it wont change what we are going to do. We will be looking at reflux. Probably wouldnt do the monitoring. We might trial of proton pump inhibitor. If you are having problems, the first two things you think about are sinusitis and GERD.

We are doing layered treatments.

* Beta-adrenergic agonists: * Beta-2 agonists are the most effective bronchodilators available * They are relatively free of unwanted effects. Shot acting beta agonists. Two puffs every four hours. You give it initially when someone omes * Two types in with an acute attack. Instead of one treatment after another, just give them continuous * Short-acting treatment. There area couple of side effects * Long-acting * Short-acting beta-2 agonists: * They are useful for symptom relief. * The frequency of administration should be taken as a guide to the patient's requirement for additional inhaled steroids. * Examples: * Albuterol Albuterol is most commonly used one. May be all you need. If someone has exercise induced * Terbutaline asthma, tell them to take 2 puffs before they go out to jog. These people with asthma should * Long-acting beta-2 agonists: never be without a rescue inhaler. * They cause bronchodilatation for more than 12 hours. * Useful for the control of symptom, when taken twice daily. Longactings work. Salmeterol has some controversy- black box warning- in pharm this is the * Use long-acting beta-2 agonists in conjunction with inhaled steroids. worst thing a drug can get. It is a total contraindication in some people to use it in certain * Examples: conditions. These drugs work, but people were using them ilke they would a rescue inhaler, * Salmeterol so these drugs take awhile to take effect and people were dying. * Formoterol * Methylxanthine: * It is used in the treatment of moderate to severe asthma. * There is a narrow margin between the therapeutic and toxic doses, and the half-life can be modified by a variety of factors, making a therapeutic dose hard to achieve. * Decreased use in current asthma management. Theophylline is not used by professor, but its used in poor countries because its cheap. It * Example: works but with sideffects. * Theophylline * Anticholinergics: * Anticholinergics prevents bronchoconstriction triggered by irritants and cold. * Agents: Ipatropium is used more in COPD than asthma, but its still a godo drug * Ipratropium bromide * Atropine General Treatment * Corticosteroids: * Inhaled steroids are used in the long-term treatment of asthma. * Therapy with inhaled corticosteroids is now recommended at a much earlier stage than previously thought. * Inhaled steroids, have minimal systemic effects. * Decrease the amount of systemic absorption by usage of metered-dose inhalers.

Some people used inhaled corticosteroids as first line, but in adults, professor would use serevant? first. But no matter what they use, these people need a short acting beta 2 agonist.

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* Mast Cell Stabilizers (Cromones): * They inhibit the early inflammatory response to allergen by stabilizing mast cells. * They inhibit the late response of airways hyper-responsiveness by an action on macrophages and eosinophils. * Cromones are less effective than inhaled corticosteroids. * They may cause fewer long-term side-effects. * Examples: * Cromolyn (Sodium cromoglycate) * Nedocromil * Leukotriene antagonists: * Selectively block the action of leukotrienes on the respiratory tract. * Reduce: * Vascular permeability * Mucus secretion * Bronchoconstriction * Eosinophil recruitment * Leukotriene antagonists: * Can be considered first-line therapy, especially in children. * Inhibit early and late stage bronchoconstriction * Has both bronchodilatory & anti-inflammatory role. * Examples: * Zileuton 5 Lipoxygenase inhibitor * Montelukast (singulair) LTD4 receptor antagonist * Zafirlukast (accolate) - LTD4 receptor antagonist

Cromolyn does not have long term side effects but not really used as much.

In some people this might be the first thign you do, gigve them this pill instead of an inhaler. So in different populations you may do things differently.

Good firstline drug in kids. Can be given before school but still put rescue agent in backpack.

Treatment of exercise induced asthma * Beta2 agonists: * Help in preventing the acute exacerbation of exercise induced asthma. * Short-acting beta2 agonists taken 5-30 minutes before exercise are the treatment of choice. * Inhaled steroids: * Work only prophylactically preventing the late-onset exercise induced asthma. * Mast-cell stabilizers: * Can be used as an alternatives to beta2 agonists. * But they are not as effective as beta-2-agonists. Management of Severe Asthmatic attack (status asthmaticus) * If life threatening features present : * oxygen (to maintain SaO2 > 92%) * inhaled 2 agonist Albuterol - Use every 20 min. Maybe given as continuous aeresol updrafts * Add anticholinergics - Ipratropium bromide aeresols * Use steroids hydrocortisone, prednisolone IV * Epinephrine/terbutaline sub cutaneous * Take chest x-ray to exclude pneumothorax, pneumomediastinum, pneumonia. * May use NIPPV to rest the pt by decreasing WOB * Transfer to ICU for/after intubation if the patient doesnt respond to above measures. After management of acute attack, step down the therapy to the lowest dose to control the symptoms & signs.

Exercise induced asthma.

Status asthmaticus is lethal condition. Even if you do everything right, patient can still die. You sometimes just cant break their bronchospasm.w hen you intubate them, you have to know what their peak airway pressures are. You can collapse the lunga nd cause their iatrogenic death right there. You want to use pressure control or increase I:E slow infusino rates, flow rates, might even use permissive hypercapnia. If they are really,r eally bad, might even treat them like an ARDs patient. Sometimes take a day or 2 to break tohe bronchospasm Ideally, first you want to give oxygen and get SaO2 above 92%. Never be afraid of giving oxygen. Despite old doctors saying you can make them stop breathing because of it. And inhaled beta agonist, thats key. If they are moderally bronchospastic, then you can just give them some bursts. -Side effects of albuterol: It will spike your sugars and decreases potassium. What does it do to nerves? They will be hanging off the light fixtures, because of how jittery you will make them. Next thing he adds is an anticholinergic. Then immediately IV steroids will be given, if they are really bad, they will be given subcut epinephrine. We are diong all these things simultaneously. If they are infected, then cover them empirically with a 3rd gen cephalosporin, etc. If we can bridge the gap without intubating them, its better for the patient. These patients must be able to protect their airway before you put them on NIPPV. Otherwise you intubate them. It will come with time as to which you can do.

Chronic Obstructive Pulmonary Disease

Definition * COPD is a chronic, slowly progressive disorder characterized by airway obstruction (FEV1 < 80% of predicted and FEV1/FVC ratio < 70%) which does not change markedly over several months. * The impairment of lung function is largely fixed but is partially reversible by bronchodilator or other therapy. * Chronic Bronchitis: * Presence of chronic productive cough for 3 months in each two successive years in a patient in whom other causes of chronic cough have been excluded. * Emphysema: * Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles and destruction of their walls without any obvious fibrosis with progressive dyspnea. Epidemiology * COPD affects 20% of adults in U.S. * It is the fourth leading cause of death in U.S. * Severity is closely associated with the number of cigarettes smoked per day. * Males are more frequently affected than females * Caucasians are more frequently affected than African Americans. Risk factors * Cigarette smoking * Domestic or occupational pollutants * Viral childhood infections * Family history of COPD * Hereditary disease: * Alpha-1-antitrypsin deficiency * Cystic fibrosis * Kartagener's syndrome - Hereditary syndrome of situs inversus (transposition) of the viscera, abnormal frontal sinuses producing sinusitis, bronchiectasis, and immobility of the cilia * Inflammatory diseases: * Rheumatoid arthritis Pathogenesis (With Picture) Chronic bronchitis: * Chronic Bronchial irritation * Increase in the size and number of mucous glands & goblet cells * Inflammatory infiltration * Occlusion of small airways by mucous and fibrosis * Hypertrophy of smooth muscles * Sometimes partial destruction of bronchial cartilage XRAY. Chronic bronchitis looks like this. Bronchi are ratty? looking with strictures & dilation. Not smooth & uniform Cartoon of obstructed broncus Emphysema * Types of emphysema according to its distribution in the lobule and acinus. * Centriacinar - Involvement of the central or proximal parts of the acini formed by respiratory bronchioles. * Panacinar - The acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli. * Distal acinar - Involvement of the distal potion of the acinus. Close to the adjacent pleura Emphysema: depends which part of the bronchial tree is being effected Emphysema

It maybe partially rev. or it may not. Even its not rev., we still treat them with the rev. treatment.

Chronic bronchitis :: 3 months of prod. Cough for 2 consec. Yrs when all the others causes have been ruled out [i.e. other cause :: GERD] COPD - small bubbles .. Develop; right sided cor pulmonale

Only 20% of smokers develop chronic bronchitis Males > females Few more caucasians

Biggest risk factor :: SMOKING But remember occupation, hereditary [alpha-1-antitryp, CF], RA!!* every disease will have one connective tissue on it

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Pathogenesis * The current opinion favors emphysema arising as a consequence of two critical imbalances. * The protease-antiprotease imbalance. * The role of alpha 1 anti-trypsin deficiency in emphysema. * 1% of all patients with emphysema have this defect. * Smoking lead to accumulation of neutrophils and macropahges secretion of elastase, & proteinase * Oxidant-antioxidant imbalance. * Tobacco smoke contain abundant reactive oxygen species which deplete the antioxidant mechanisms tissue injury. * Oxidative injury inactivation of native antiprotease damage of alveoli. Pathogenesis - Emphysema * Initially, the alveolar destruction occurs near respiratory bronchioles. * With the progression of the disease, the entire lobule may be destroyed. * Terminal air spaces are enlarged. * Lungs elastic recoil is reduced. * The airways collapses during expiration. * The consequences of the expiratory limitation are: * Increase in residual volume and lung hyperinflation * Decrease in inspiratory capacity * The hallmark of COPD is reduction of maximal expiratory flow rate. Schematic of Emphysema and Chronic Bronchitis Clinical Features * Predominant Chronic Bronchitis (blue bloater): * Symptoms: * Cough and sputum - mucoid or mucopurulent * CO2, O2, cyanosis * Edema * Signs: * Hyperinflated chest * Reduced expansion on palpation * Hyper-resonance * Decreased breath sounds with end-expiratory wheezes and early inspiratory crackles Clinical Features * Predominant Emphysema (pink puffer): Seen more in thin and often elderly patient * Symptoms: * Dyspnea, Tachypnea * Pursed-lip breathing * Scanty sputum production * Absence of cyanosis adequate gas exchange * Signs: * Chest hyperinflation with reduced chest expansion * Hyper-resonance, and decreased breath sounds * Cor pulmonale is infrequent * Wide variation in presentation most patients cant be classified as just blue bloaters or Pink puffers Muscle wasting see residual volume go WAY up; the tidal volume is not changing as much; increase dead space Complications of emphysema * Spontaneous pneumothorax caused by rupture of an emphysematous bulla especially in distal acinar type of emphysema * Pneumonia * Acute bronchitis Spont. Pneumothorax. Cant see the diaphragm or lung markings on the right - this is a tension pneumothorax; air coming in & cant go back out Investigations * Pulmonary function tests: * Obstructive pattern: FEV1 * FEV1/FVC - FEV1/FVC <0.7 * Arterial blood gases: * Pink puffer: * Close to normal blood gases * Blue bloater: * Hypercapnia * Hypoxemia * Elevated bicarbonate * CBC: * Polycythemia Investigations * Radiographic studies * X-ray chest * CT scan is the definitive test for establishing presence of emphysema * Patient presenting <50 yr serum 1-antitrypsin levels XRAY. bronchi are thick edematous with smooth ms. Hyperplasia. Once again we have a horizontal heart. hyperinflation Emphysema. no lung parenchyma Emphasematous Bullae. End stage emphysema looks like this with LOTS of huge bubbles or blebs; prolly just 25% of this lung parenchyma that is still working Management of COPD * Beta2 agonist * Anticholinergics * Theophylline * Low-flow oxygen at night and with exertion; may be needed around the clock at later stages * Leukotriene receptor antagonists * Consider trial of inhaled corticosteroids Management of COPD * Treat CHF diuretics, ACE inhibitors * Pulmonary rehabilitation education and cardiovascular conditioning * Vaccinate against influenza & pneumococcus * Reduce stress or anxiety * Treat alpha1 anti-trypsin deficiency with alpha1- protease inhibitor augmentation therapy Other Therapies * Smoking cessation: * It cannot restore loss of lung function, but can prevent the accelerated decline seen in many patients with COPD. * Approaches: * Pharmacotherapy * Repetitive counseling * Educational material Other Therapies * Surgical lung resection: * Lung volume reduction surgery: * Promising but controversial * Estimation of remaining lung function after surgery is essential. * Patients with upper lobe emphysema are likely to benefit

Think about imbalances of proteases & oxidation & antioixdation. Normal repair mechanism of the tissue is LOST!!**

You lose parenchyma. Dead space increases & ultimately pulm. HTN

HALLMARK :: reduction of flow rates because of the los of recoil; their dead space goes WAY UP!!!

Cough, cyanosis, edematous airways, hyperinflated & big chests, hyperresonnant; You'll have decreased breath sounds & early crackles [because of mucous sitting in the airways ] wheezing [cuz of the collapsing airways]

Usually they're not going to have that productive cough; mostly DRY cough usually; Usually not cyanotic till the late stage; they're generally pink in the beginning They can develop cor pulmanale.. But Much more common in CHRONIC bronchitis

Pneumothorax, pneumonia, acute bronchitis; If you get somebody with LV disruption & COPD --> make for very difficult treatment; treat both of them at the same time

Pulm. Func test :: dont do this in the acute setting; hallmark is a decreased ratio of FEV1 to FVC. COPD-ers may become hyper capnic later on

A lot of these people get CT scan --> to look at parenchyma If you see emphysema in a younger person, DEFINITELY get a alpha 1-antitrysin

Walk them up & down the hall & if their stats are below 90 --> give them oxygen; they will become hypoxic at night so you might use oxygen at night .. Or might use them when they're walking around You can try Leukotriene inhibitors & try inhaled corticosteroids if you maximized the other drugs [expensive]

Make sure they dont have underlying edema that is making their situation worst Education & conditioning Make sure they get vacinated; some of these folks will improve with a lil bit of mild anxiety reducers [maybe a tiny dose of xanthrax] Alpha-1-antitrypsin Smoke cessation - its difficult for these people to quit

This is controversial; what they do is take a person with really bad COPD. They'll go in & resect the lobe out & allow the lower lobe to expand UP. He's seen it work.. & seen it fail Very few of these people ever get lung transplants

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* Patients with upper lobe emphysema are likely to benefit * Lung transplantation: * Indicated in FEV1 < 25 %, PaCO2 > 55 mm Hg and cor pulmonale Treatment of acute exacerbation of COPD * Inhaled Beta agonists - albuterol * Antibiotics common bacteria includes S.Pneumoniae, H. Influenzae, Morexella Catarrhalis, Mycoplasma and Chlamydia * Perform sputum culture and sensitivity * Glucocorticoids usually for 2 weeks * Oxygen To keep arterial saturation 90% * Mechanical ventilation may be needed in severe cases (PCO2 > 45 mm of Hg) Alpha1-antitrypsin (AAT) deficiency * Alpha1-antitrypsin (AAT) deficiency, is one of the most common inherited disorders among Caucasians * Affects 1 in 3000-5000 individuals in US * Its primary manifestation is early-onset panacinar emphysema * About 1-3% of patients with diagnosed COPD are predicted to have AAT deficiency AAT- pathogenesis * AAT is synthesized in liver * The major biochemical activity of the AAT molecule is inhibition of several neutrophil-derived proteases (eg, trypsin, elastase, proteinase 3, cathepsin G). * The production of alpha1-antiprotease is controlled by a pair of genes at the protease inhibitor (Pi) locus * Nearly 24 variants of the alpha1-antiprotease molecule have been identified AAT- pathogenesis * The most common (90%) allele is M (PiM), and homozygous individuals (MM) produce normal amounts of alpha1-antiprotease (serum levels of 20-53 mmol/L or 150-350 mg/dL). * The most common form of AAT deficiency is associated with allele Z, or homozygous PiZ (ZZ). * Serum levels of AAT in these patients are about 3.4-7 mmol/L, 10-15% of normal serum levels. * Emphysema develops in most (but not all) individuals with serum levels less than 9 mmol/L. Clinical features * Dyspnea develops by 30-40 yrs age * Wheezing - sometimes * Signs of emphysema develop barrel shaped hyper-inflated chest * Cigarette smoking accelerates the progression of emphysema in patients with AAT deficiency * Impaired liver function in some patients and may lead to cirrhosis and liver failure (15%) Lab diagnosis * Serum AAT levels - Levels less than 80 mg/dL suggest a significant risk for lung disease * Genotyping - is required to confirm AAT deficiency * Imaging and pulmonary function tests (similar to emphysema) Treatment * Quit smoking * Bronchodilators - Beta agonists, cholinergics, corticosteroids * Prevention of infections annual penumococcal and influenza vaccines * Enzyme replacement - AAT-deficient individuals who have or show signs of developing significant emphysema can be treated with Prolastin, (a pooled, purified, human plasma protein concentrate for alpha-1 antitrypsin) * Surgical treatment a) Volume reduction and b) lung transplantation

Very few of these people ever get lung transplants Same thing you do for asthma but prolly going to use more antiBiotics; Whether its asthma or copd, they'll prolly get antibiotics even if they need it or not;[levikin would be a good choice] Remember to keep their stats up; sometimes we have to intubate them & rest them Avg. chronic bronchitis pts, come in atleast 5 times a yr; they're so glad when they can get breathing done for them but the problem with that is its very difficult to get them to ween off of this!! Need good weening strategies to get them back off [have to build up their resp. muscles] Always ask yourself, when these people come in WHY!?! Its not enough to make the diagnosis. Its not just the diagnosis, need to know WHY they had these aspirations [infection, mi --> edema --> copd, pneumothorax] Alpha 1 - early onset! NOT asking us about the genetic component of this! Genetically inherited imbalance If you have emphysema in a pt. that is super young, that's hwen you want to check this; cigarrette smoking makes it WORSE! IF you have early onset of emphysema --> liver cirrhosis

Ct of their chest. Then a pulm. Function test

Infuse prolastin [continuous infusion] - very very expensive; these people are GOOD transplant recipients

Think about what they have & How are they similar, different, how you treat them [chronic treatment vs. acute setting]

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