Class 23 review Flashcards
Asthma
Asthma is a chronic inflammatory disorder of the airways. When the airways become inflamed, some obstruction of airflow occurs and we will see symptoms like breathlessness, coughing, wheezing, chest tightness. The airways become hyper-responsive to certain triggers that can bring on an asthma attack.
Diagnosis of asthma
spirometry
exacerbation
When a person with COPD has a sudden increase in symptoms. Symptoms are worse for a period of time and then may improve. Exacerbations are often precipitated by respiratory illness such as colds, pneumonia and influenza. Exacerbations of COPD are frequently the cause of hospitalization. Dyspnea, cough, sputum
Asthma triggers
Allergens
Exercise
Respiratory infection
Nose & sinus problem
Drugs (NSAIDS, beta blockers)
GERD
Air pollutants
Emotional stress
Early phase response of asthma
Bronchospasm. Increased mucus secretion, edema formation, and increased amounts of sputum
30-60 min
Late phase response of asthma
Primarily inflammation
Peaks 5-12 hrs
Corticosteroids are effective in preventing and reversing this cycle
If not treated, may lead to irreversible lung damage
Asthma clinical picture
Obstruction & air trapping
Dyspnea & chest tightness
Speech 1-2 words
Anxiety, distress
Tachycardia
Initially low O2 low CO2
SABAs - Inhaled
B-Adrenergic agonists
- prevent release of inflammatory mediators from mast cells
- SABAs not for ongoing long-term use
- onset of action in minutes and duration of 4-8 hr
SABAs example
Salbutamol (Ventolin)
LABAs - Inhaled
- long-acting: take q12h
- used for long-term control asthma
- control - not a rescue inhaler
- works by same mechanisms as SABAs
- can be combined with inhaled corticosteroid (ICS) (fluticasone)
LABAs example
Salmeterol (Serevent diskus)
Anticholinergic - Inhaled
- block action of acetylcholine
- usually used in combination with another bronchodilator
- most common adverse effect is dry mouth
Anticholinergic example
Ipratropium (Atrovent)
Methylxanthines
- less effective long-term bronchodilator
- controller after trying ICS, LABA, and LTRAs
- Narrow toxic/ therapeutic ratio and frequent adverse events
Methylxanthines example
Theophylline
Corticosteroids
- decreases inflammation in airways by suppressing immune response
- reduce bronchial hyper-responsiveness
- decreases mucus production
- are taken on a fixed schedule
- oropharyngeal candidiasis, hoarseness, and a dry cough are local adverse effects of inhaled drug
- adverse effects can be reduced by a spacer or gargling after use
- taken daily, not a rescue drug
Corticosteroids examples
Inhaled: fluticasone (Flovent)
Systemic: prednisone
Leukotriene modifiers or inhibitors
- block action of leukotrienes - which are potent bronchoconstrictors
- have both bronchodilator and anti-inflammatory effects
- not indicated for acute attacks
- used prophylactic and maintenance therapy
- taken daily not a rescue drug
Leukotriene modifiers or inhibitors example
montelukast (Singulair)
Mast cell stabilizers
- alternative to corticosteroids if needed
- inhibits release of histamine from mast cells to reduce inflammation
- may cause local irritation in nose, mouth, throat
- taken daily not a rescue drug
Mast cell stabilizers example
Cromolyn
COPD
Chronic obstructive pulmonary disease
- disease caused by smoking 80-90%
- progressive partially reversible airflow obstruction
- increasing frequency & severity of exacerbations
- characterized by chronic inflammation found in the airways, lung parenchyma, and pulmonary blood vessels
COPD risk factors
Cigarette smoking
Occupational chemicals and dust
Air pollution
Infection
Heredity
Aging
COPD and smoking
- COPD ~ age 50 or ~20 pack years
- 15% of smokers develop clinically significant airway obstruction
- 80% to 90% of COPD deaths are related to tobacco smoking
Emphysema
Destruction of alveoli and permanent enlargement of airways without fibrosis
Chronic bronchitis
Over-secretion mucous and chronic productive cough that lasts more than 3 months for a minimum 2 years in a row
COPD pathophysiology
Air is trapped inside the lungs which causes hyperinflation and overexpansion
Mucus hyper secretion
Airflow limitation
Loss of elastic recoil
Pulmonary hypertension
COPD clinical manifestations
Underweight with adequate caloric intake
Anorexia
Chronic fatigue
Bluish-red colour of skin
- polycythemia and cyanosis
Prolonged expiratory phase
Wheezes
Decreased breath sounds
Barrel chest
Cor Pulmonale pathophysiology
Hypertrophy of right side of heart
- Result of pulmonary hypertension
- Late manifestation of chronic pulmonary heart disease
- Eventually causes right-sided heart failure
Cor Pulmonale symptoms
Dyspnea
Distended neck veins
Hepatomegaly with rihgt upper quadrant tenderness
Peripheral edema
Weight gain
Ascites
Epigastric distress
Salbutamol (Ventolin)
Short acting: 3-5 hourss
Activate beta 2 adrenergic receptors in the pulmonary smooth muscle, causing bronchodilation.
Also may suppress histamine release
Salmeterol (Serevent diskus)
Long-acting: 12 hours
Used for long-term control of chronic COPD.
Works by same mechanism as SABAs
Ipratropium(Atrovent)
Short-acting muscarinic antagonist (6 hours)
Blocks muscarinic receptors in the bronchi, which decreases and prevents further bronchoconstriction
Tiotropium (Spiriva)
Long-acting muscarinic receptor (24 hours).
Works in the same mechanism as Ipratropium but is more effective
ICS Fluticasone (Flovent) or Beclomethasone
Decreases inflammation in airways by suppressing immune response.
Not to be used alone in COPD, used with a LABA.
Asthma diagnosis
test for reactivity
Methacholine Challenge (histamine)
Exercise Challenge
Drop by 15 – 20% of FEV1 indicates hyper-responsive airways
- Allergy testing
- Sputum eosinophils
- Sputum culture and sensitivity
COPD diagnosis
test for obstruction
Reduced FEV1/FVC ratio
Increased residual volume COPD is diagnosed when FEV1/FVC is less than 70% predicted
- Walk test (6 min.) to determine O2 desaturation in the blood with exercise
- ECG can show signs of right ventricular failure
Carbon dioxide Narcosis
a tolerance for high levels of carbon dioxide and development of a “hypoxic drive” to breath
Monitor: cognitive changes and physical assessment
Oxygen Toxicity
high concentrations of oxygen can damage alveolar-capillary membranes
Absorption Atelectasis
high oxygen washes out nitrogen from alveoli → alveolar collapse
