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30 Cards in this Set
- Front
- Back
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Name the most common causes of bronchiolitis.
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#1 RSV; mycoplasma pneumoniae
smoke/sulfur dioxide hypersensitivity pneumonitis collagen vascular disease immunodeficiency drug reaction bronchiolitis obliterans |
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When is RSV season?
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October to May
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What happens/causes bronchioliits?
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necrosis of respiratory epithelium-- mucus plugging and submucosal edema. This results in narrowing and obstruction of the airways.
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When do symptoms peak in bronciolitis?
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3-5 days, last 2 weeks
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What populations are at high risk for bronchiolitis?
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premies
congenital heart disease immunodeficiency bronchopulmonary dysplasia |
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What causes croup?
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80% is parainfluenza virus (1>2,3)
RSV Adenovirus Influenza, rhinovirus, enterovirus |
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What virus causes the most severe cases of croup?
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Influenza A
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What is croup?
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Inflammation of the larynx and subglottic airway.
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When is croup most common?
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6mo-3yr
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What do you see on x-ray in someone with croup?
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steeple sign = subglottic narrowing
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How do you treat croup?
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dexamethasone 0.6mg/kg im or po (t1/2 is 54hr)
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What is the most common genetic mutation seen in CF?
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CFTR delta F508 (absence of phenylalanine)
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What are the clinical features seen in CF?
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1. sinuses- CRS with polyps, AFS
2.Pulm- recurrent pna pseudo/staph;ABPA; bronchiectasis 3. GI: FTT, malabsorption, diarrhea, meconium ileus, small bowel obstruction, focal biliary cirrhosis, pancreatic exocrine insufficiency 4. Reproductive- azoospermia; 5. skin-- salty 6. musculoskeletal-- clubbing, hypertrophic osteoarthropathy 7. renal- nephrolithiasis, nephrocalcinosis |
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What is the estimated frequency of CF in caucasians? african americans? native americans?
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caucasian= 1/2000
AA= 1/17,000 Native American= 1/80,000 |
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How do you make the diagnosis of CF?
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one organ system affected + evidence of CFTR dysfunction. (elevated sweat chloride, >2 mutations in CFTR, or abnormal nasal potential difference)
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What value indicates an abnormal sweat chloride?
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>60 Eq/L
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How do you treat CF?
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chest PT; physical training
Recobinant Human Dexoyribonuclease; Hypertonic Nebs Antibiotics; Oxygen Lung transplant- 50% 2 yr survival Fat soluable vitamins high calorie diet |
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What are the 3 components of airway mucus?
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1. Sol layer: watery mixture in direct contact with airway epithelial cells
2. Gel layer: elastic layer in direct contact with inhaled air 3. Proteins: mucin glycoproteins, proteoglycans |
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What are the 3 key cells in mucociliary clearance?
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1. Goblet cells: secrete mucus
2. Clara cells: nonciliated secretory cells, in terminal bronchioles (goblet precursor?) 3. Submucosal gland cells: nonciliated collecting duct and secretory tubules, lined by mucus and serous cells |
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How do you measure nasal mucociliary clearance time/
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place a particle of saccharin on mucosa of the inferior turbinate and measure time till you can taste it (sweet).
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Describe/draw cilia's structure.
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shaft anchored to cytoplasm;
contain longitudinal fibrils composed of 9 outer pairs of doublets and 2 central microtubules; Dynein arms join adjacent doublets. |
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What effects does a defect in MUC5A have on asthmatics?
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causes airway mucus to be quantitatively/qualitatively abnormal. Increased albumin and DNA are increased leads to mucus accumulation and obstruction.
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What gene is affected in CF? What effect does it have?
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CFTR (cystic fibroris transmembrane regulatory gene); defect causes decreased serous cell secretion of water important for mucin hydration. Cilia structure and beat are normal.
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What is the defect in primary ciliary dyskinesia?
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lack of dynein arms, defective cilliary spokes.
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What is Karagener's Syndrome?
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primary ciliary dyskinesia and situs inversus (50% of PCD pts) *ciliary movement is important for organ orientation during fetal development.
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Does ciliary function decrease life expectancy?
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No (unlike CF)
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What is the mucin gene?
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MUC5A
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What disease state has an increased expressin in MUC5A (mucin gene)?
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Asthma
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List the 9 airway changes that occur in asthmatic patients during airway remodeling.
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1. Surface epithelium is denuded/fragile.
2. Reticular basement membrane is thickened (hyaline) 3. Mucous cell metaplasia 4. Bronchial smooth muscle enlargement in LARGE airways 5. CD3/CD4 cell infiltrate with IL 2R (CD25), eosinophilia, increase in mast cells 6. Increase in IL-4, IL-5 gene expression 7. Variable reversible airflow obstruction 8. Post mortem see airway plugs, hyperinflation. NO empysema. |
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List the 9 airway changes that occur in COPD patients during airway remodeling.
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1. Surface epithelium is normal.
2. Reticular basement membrane is variably thickened (hyaline) or NL 3. Mucous cell metaplasia or hyperplasia 4. Bronchial smooth muscle enlargement in SMALL airways 5. CD3/CD8 cell infiltrate with IL 2R (CD25), VLA-1, HLA-DR+, mild increase in eos, mast cells 6. Increase in GM-CSF, +/- IL-4 gene expression. No IL-5. 7. Progressive increase in airway obstruction 8. Post mortem see prominent emphysema, more small airway involvement, excessive mucus. |
