respiratory diseases pt 2.txt

• a collection of symptoms in the nose and eyes due to exposure to an allergen
• allergen exposure causes release of numerous mediators such as histamine and leukotrienes

• dust
• dander
• mold
• pollen
• mites
• cockroaches

• Histamine 1 (H1) receptor antagonists
• Glucocorticosteroids
• alpha1-adrenergic receptor agonists (decongestants)
• leukotriene receptor antatgonists

• blocks H1 receptors
• oral or intranasal spray
• treats: rhinorrhea, sneezing, nasal pruritis & nasal congestion

• sedation
• dry mouth

• inhibit release of mediators from inflammatory cells
• intranasal spray
• treats: sneezing, nasal pruritis, nasal discharge & nasal congestion

tend to be minimal due to limited systemic exposure (nasal spray)

• activate alpha1-adrenergic receptors causing vasoconstriction of blood vessels in nose, throar and sinuses
• oral or intranasal spray (not to be used for more than 3 days)
• treats: inflammation, nasal swelling & mucus production

increased systemic blood pressure, tremor, tachyphylaxis, nausea, vomiting, weakness & headache

• block leukotriene receptors
• oral roue of administration
• treats: nasal secretions, nasal congestion & vasodilation

vomiting, diarrhea & headache

• chronic inflammation of the lungs
• lungs exhibit structural changes
• compromised respiratory gas exchange
• diseases include: asthma, chronic bronchitis, emphysema, pneumoconiosis

• characterized by reduced lung volume
• increased lung stiffness (decreased lung compliance)
• disease of lung parenchyma, pleura, chest wall or neuromuscular apparatus
• diseases include: pulmonary fibrosis, lung cancer, pneumonia

• inflammatory disorder of the airways
• three types: allergic, exercise-induced and occupational

• wheezing
• shortness of breath
• chest tightness
• coughing

• allergic - triggered by allergens
• exercise-induced - worsens when breathing cold, dry air during exercise
• occupational - caused or worsened by breathing in a workplace irritant such as chemical fumes, gases or dust

• airway obstructors
• airway inflammation
• airway hyperresponsivemess
• airway remodeling

• starts withing seconds, lasts ~1 hour
• caused by release of preformed mediators such as histamine, prostaglandins, thromboxane A2
• clinical response includes smooth muscle contraction, airway obstruction and increased microvascular permeability

• takes up to 6-12 hours to develop
• caused by the induces synthesis of mediators including leukotrienes, chemokines and cytokines
• clinical response includes smooth muscle contraction, airway obstruction, edema and airway hyperreactivity to bronchoconstrictory stimuli such as histamine and methacholine

• combined inhaled glucocorticosteroid and long acting beta2-adrenergic receptor agonist
• inhalded glucocorticosteroids (alone)
• leukotriene receptor antagonists
• inhaled beta2-adrenergic receptor agonists (alone) (short and long acting both)
• monoclonal antibody, omilizumab (Xolair), blocks a pathway that the immue system uses to trigger asthma
• mast cell stablizers
• Methylxanthine derivatives
• inhaled muscarinic receptor antagonists

• inflammation of the bronchi
• excessive secretions of mucus into the airways
• airway narrowing of airway closure
• two types: acute and chronic

• cigarette smoking (#1 cause)
• industrial fumes
• automobile exhaust
• microorganisms - bacterial or viral bronchitis

persistent or prolonged: chest pain, dyspnea, cough, fever & chills

• rhonchi (gurgling sounds during inspiration/expiration)
• hypercapnia (elevated blood CO2 levels)
• hypoxemia (decreased blood O2 levels)
• respiratory acidosis

• combined inhaled glucocorticosteroid and long-acting beta2-adrenergic receptor agonist
• inhaled glucocorticosteroids (alone)
• inhaled beta2-adrenergic receptor agonists (alone) (short acting "rescue" and long-acting)

• involves damage to the lung air sacs affecting breathing, leading to:
• progressive destruction of alveoli and the surrounding lung tissues
• air trapping in the lungs due to a lack of supporting tissue, thus decreasing blood oxygenation
• with advanced emphysema, large air cysts develop in the place of normal lung tissue causing atelectasis (collapse of part or all of a lung)

• smoking (#1 cause)
• alpha1-antitrypsin (AAT) deficiency

• second and possibly third-hand smoke contributes to emphysema in non-smokers
• 4,000 chemicals in tobacco smoke
• chemicals slowly destroy the small peripheral airways, the elastic air sacs and their supporting elastic fibers

• ~1-2% of people have inherited form involving a deficiency in the protein AAT
• AAT is a protease inhibitor made in the liver
• AAT protects the elastic structures in the lungs from enzymes that can progressive lung tissue
• AAT also protects the liver
• Early onset emphysema (between 30-40) may occur in a smoker with a lack of AAT

• shortness of breath
• wheezing
• chest tightness
• reduced capacity for physical activity
• chronic coughing
• loss of appetite
• fatigue
• cyanosis

• combined inhaled glucocorticosteroid and long-acting beta2-adrenergic receptor agonist
• inhaled muscarinic receptor antagonists
• supplemental O2 therapy
• pulmonary rehabilityation program (combines education, exercise training and behavioral intervention to stay active an improve health and quality of life)
• lung volume reduction surgery (LVRS) - removal of diseased lung wedges to help remaining tissue work more efficiently and improve breathing

an inherited autosomal recessive disease that causes thick, sticky mucus to build up in the lungs and digestive tract

• coughing or increased mucus production in the sinuses or lungs
• nasal congestion and/or sinus pain or pressure caused by infection or nasal polyps
• increased shortness of breath
• fatigue
• recurrent episodes of pneumonia
• fever
• loss of appetite

• antibiotics to prevent and treat lung and sinus infections
• inhaled beta2-adrenergic receptor agonists with chest percussion, postural drainage and breathing control exercises
• DNAse replacement therapy to thin mucus and make it easier to cough up
• flu vacine and pneumococcal polysaccharide vaccine (PPV) yearly
• supplemental O2 therapy
• lung transplant

• results from inhaling particulate matter over a long period of time
• particulate matter triggers lung inflammation causing lung damage
• remodeling occurs forming tough, fibrous tissue deposits in damaged lung areas
• fibrosis stiffens the lungs and interferes with O2 and CO2 exchange

• Coal Worker's pneumoconiosis
• Talc pneumoconiosis
• asbestosis
• silicosis
• Kaolin (china clay) pneumoconiosis

• chronic cough
• shortness of breath, especially with exercise
• wheezing
• low physical endurance

• combined inhaled glucocortiosteroid and long-acting beta2-adrenergic receptor agonist
• supplemental O2 therapy

inflammatino of the pleural linging of the lungs and chest

• pneumonia
• tuberculosis
• chest trauma
• tumor formation

• pain in the chest during deep breathing (inhale or exhale)
• cyanosis
• coughing
• shortness of breath
• tachypnea

• removal of fluid in the lungs by thoracentesis
• antibiotics for bacterial infections; may require a surgical procedure to drain infected fluid
• NSAIDs