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21 Cards in this Set
- Front
- Back
Asthma medications: bronchodilator continued |
Anticholinergic: ipratropium and tiotropium bromide :blocks neurotransmitter acetylcholine :ATROVENT OK WHEN FIRST LINE BRONCHODILATORS ARE INEFFECTIVE, OR THE PATIENT HAS AN ADVERSE REACTION TO B2 AGONIST (INCREASE HR) :MAY ALSO BE USED IN COMBINATION W/BETA ADRENERGICS :ipratropium + albuterol (combivent MDI, Duoneb: svn) called a synergistic relationship cause the two meds work together to help the patient. |
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Asthma medications: Bronchodilators Cont |
Methylxanthines/Xanthines :Less effective than beta adrenergics :naturally occurring in body :phosphodiesterease inhibitors :Backdoor bronchodilator :Oral, injection, suppository form NOT FOR USE IN EMERGENCY/ ACUTE ATTACK theophylline is a methylxanthine, methylxanthines/Xanthines are found in coffee, cocoa, anything with caffeine. |
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miscellaneous asthma factoids |
People who use too many bronchodilators (wear out the key/lock mechanism, B2 agonist/receptor) Status asthmaticus refractory to bronchodilators: emergency Use aggressive bronchodilators and early use of corticosteroids possibly IV May need (positive airway pressure)PAP or Heliox(helium and oxygen mixed) to force medication(controvery cause denser gases to deliver medications works better, meaning how far down the drops get in airway depends on density of gas, helium is less dense, might not get far) Bronchial thermoplasty: heat via radio lessen ability to constrict smooth muscle. Dilates airways 5 years, nearly 80% success. Not for emergency |
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Endotracheal intubation if nothing else works Homework pages 200 to 208 Jardins Page 535 and 953 Egan |
Trachea is distal to the esophagus. trachea is on the outside for breathing. |
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Bronchiectasis |
bronchiectasis is destruction and widening of the large airways :may be congenital or acquired (not hereditary per say) Bronchiectasis is often caused by recurrent inflammation or infection of the airways Cystic fibrosis causes about a third of all bronchiectasis cases in the united states Would want antibiotics and mucolytics |
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Bronchiectasis |
May be caused by congenital DZ named Kartagener's syndrome, autosomal recessive, dyskinesia of cilia Influenza and other pulmonary infections can lead to acquired bronchiectasis Possible but not typically associated with COPD Often PT has right sided heart failure due to hypoxemia and PHT pulmonary hypertension |
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Bronchiectasis definition |
A chronic necrotizing infection proximal to bronchi and bronchioles leading to , or associated with, abnormal dilation and destruction of the larger airways. |
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Bronchiectasis |
3 major types 1. varicose: twisted, distorted bronchi resembling varicose veins 2. cylindrical: bronchi are twisted and resembles tubes 3. Saccular (cystic) bronchi end in large cyst like sacs |
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Radiologic findings |
Chest radiograph :translucent (dark) lung fields :Depressed or flattened diaphragm :Hyperinflation: mucous plugs :long and narrow heart Air bronchograms (air filled sacs) |
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Pathological changes |
Hallmark is chronic production of large quantities of purulent fetid sputum Depending on extent, restrictive or obstructive :dyspnea :Hemoptysis :dull or tympanic percussion :wheezing, rhonchi, crackles :Atelectasis, consolidation |
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Abnormal laboratory tests and procedures |
Polycythemia Sputum examination :Streptococcus pneumoniae :Haemophilus influenzae :Pseudomonas aeruginosa :Anaerobic organisms :DZ less occurrence today due to antibiotic therapy advancements. |
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General management of bronchiectasis |
Respiratory care treatment protocols :#1 antibiotics and expectorants :Immunizations against infectives :Bronchopulmonary hygiene therapy protocol :Bronchodilator protocol :Hyperinflation therapy protocol :Mechanical ventilation protocol :Surgery, lung resection. Quiz on asthma and bronchiectasis |
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Cystic fibrosis |
Chapter 34 page 705 to 797 EgansChapter 14 page 213 des jardins |
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CF Case study |
Answer self assessment questions 1 to 10 in Jardins page 249. |
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Cystic fibrosis |
Etiology Cystic fibrosis is an inherited childhood disease that causes thick, sticky mucous to build up in the lungs and digestive tract It is a multi system involving disease |
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Etiology |
CF is a genetic DZ 2 defective genes to be passed down (autosomal recessive) : one from each parent Over 1000 different mutations 1:1000 births caucasians americans have the CF gene Approx 30000 in the use 1000 new each year Average of survival today is 37 to 40 years old |
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Facts |
Most children are diagnosed with CF by their 2nd birthday. A small number, however are not diagnosed until age 18 or older. These patients usually have a milder form of CF. |
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Anatomical alterations |
Thick viscid secretions inrespiratory tract Clogs pancreatic ducts Clogs bile ducts in liver Mucosal inflammation Mucosal hypertrophy Recurrent LRTI (lower respiratory tract infection) Bronchiectasis Obstructive DZ |
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Cllinical manifestations |
Excessive mucous production Reoccuring infections (pseudomonas aeruginosa) Hemoptysis (bronchiectasis) Pulmonary hypertension(hypoxia and pressure against capillary beds) Respiratory failure Stunted growth (inability to properly digest food) |
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CF clinical testing |
#1 increased chloride content in sweat (sweat test) Salty taste when kissed Increased salt wasting Dehydration in hot weather Salt craving Newborn genetic testing :sweat test to verify |
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CF radiology |
Chest X ray :hyperinflation :peribronchial thickening :Lung collapse: atelectasis Chest CT (computed tomography) :Bronchiectasis :mucoid impaction :Areas of centrilobular opacities :sub pleural bullae (fluid filled sacs like blisters, develop on the lung parenchyma under the visceral plueral) |