Showing posts with label Pathophysiology. Show all posts
Showing posts with label Pathophysiology. Show all posts

Thursday, September 26, 2013

Pathophysiology for Asthma

• Asthma is increased bronchial reactivity in the lower respiratory tract to various stimuli, which produces episodic bronchospasm and airway obstruction and inflammation.
• It is the most common respiratory disease in children. In younger children, it affects twice as many boys as girls and evens out by adolescence.
• Immunologic/allergic reaction results in histamine production causing edema of the mucus membrane, spasm of the smooth muscle of bronchi and bronchioles, and accumulation of secretions.
• Asthma can be intrinsic (allergen is not obvious) or extrinsic (results from sensitivity to specific external allergens).


Etiology:
• Extrinsic asthma: exposure to pollens, animal dander, house dust or mold, feather pillows, silky materials, food additives.
• Intrinsic asthma: irritants, emotional stress, fatigue, endocrine changes, temperature and humidity changes, and exposure to noxious fumes.


Precipitating/risk factors:
• Allergen
• Upper airway infection
• Sudden change in temperature or weather
• Exercise, anxiety, excessive coughing, or laughing


Signs and Symptoms:
• Sudden dyspnea, wheezing, and tightness in the chest
• Coughing that produces thick, clear, or yellow sputum
• Tachypnea and use of accessory respiratory muscles
• Rapid pulse, profuse perspiration, hyperresonant lung fields, diminished breath sounds
• Barrel chest appearance from chronic air trapping
• Irritability from hypoxia


Diagnosis:
• Physical examination
• Chest X-ray: hyperinflated lungs with air trapping and local atelectasis during attacks, normal during remission
• Sputum: presence of Cruschmann’s spirals (casts of airways), eosinophils
• Skin testing for specific allergens may be necessary if the client lacks history of allergy


Treatment:
• Treatment is usually tailored to individual client’s need and focuses on identifying and avoiding predisposing factors. Desensitization of specific antigen may be helpful, but is not effective in persistent asthma.
• Emergency treatment: Oxygen therapy, corticosteroids, and bronchodilators such as subcutaneous epinephrine, IV theophylline, and inhaled agents such as metaproterenol, albuterol, and ipratropium
• Medication:
—Bronchodilators
—Beta-adrenergic agonists: metered does inhaler—children will need spacers, nebulizer—for infants and toddlers, and rescue drugs for acute attacks.
—Corticosteroids: oral for persistent wheezing, inhaled by MDI or nebulizer, IV in the hospital
—Nonsteroidal anti-inflamatory agents: nedocromil, cromolyn sodium, and leukotriene inhibitors
—Other commonly used medications are as follows:
â–  Rapid-acting epinephrine
â–  Aminophylline
â–  Terbutaline
â–  Theophylline
â–  Corticosteroids


Step Approach to Asthma Management
Step 1 Long-term control: none
Rescue (Short-term control): short-acting bronchodilator (inhaled beta 2 agonist); if used more than biw; long-term control required.


Step 2 Long-term control: daily anti-inflammatory: low dose inhaled corticosteroid or cromolyn or nedocromil
Rescue: short-acting bronchodilator (inhaled beta 2 agonist); if used daily or with increased frequency, additional long-term therapy is needed.


Step 3 Long-term control: daily anti-inflammatory: medium dose inhaled corticosteroid or low to medium dose inhaled corticosteroid plus long-acting bronchodilator (inhaled or oral). If needed, medium to high dose inhaled corticosteroid plus long-acting bronchodilator.
Rescue: short-acting bronchodilator (inhaled beta 2 agonist); if used daily or with increased frequency, improved long-term therapy is needed.
—High-dose inhaled corticosteroid plus long-acting inhaled bronchodilator or oral corticosteroid (2 mg/kg/d) and long-acting beta 2 agonist tablets.
—Rescue: inhaled short-acting beta 2 agonist
• Place the client on semi-Fowler’s position
• Administer oxygen
• Encourage diagrammatic breathing
• Administer medication and IV therapy as ordered
• Provide humidification and hydration to loosen secretions
• Monitor for respiratory distress
• Provide chest percussion and postural drainage once symptoms improve
• If the attack was caused by exertion, have the client sit down, rest, and sip warm water if not contraindicated
• For status asthmaticus, humidified oxygen to achieve full saturation; large, frequent doses of inhaled short-acting beta 2 agonists; continuous treatment with bronchodilators until clinical improvement or toxic side effects occur; subcutaneous epinephrine for those refractive to beta 2 agonists


Sunday, September 22, 2013

Pathophysiology of Meniere’s Disease

Etiology: Usually idiopathic.


S&S: Recurrent episodes (20 minutes to several hours) of spontaneous rotary vertigo, fluctuating hearing loss, tinnitus, and a feeling of fullness in the ear, often accompanied by nausea, vomiting, and sweating and sometimes loss of consciousness. After acute symptoms subside, balance is poor and client feels unwell for up to 24 hours


Rx: Low-salt diet, betahistine hydrochloride and a mild diuretic given to reduce number and severity of attacks; vestibular sedative such as prochlorperazine to abort acute attacks. Surgery may be done in refractory cases.


Nursing Process Elements
Help the client identify precipitating events or forewarning of attacks


Client teaching for self-care
• Aim to reduce severity of attacks by taking medication as prescribed when attack starts and lying down on the unaffected side in a quiet, darkened room and avoiding sudden movements and activities including reading
• Try to prevent attacks by avoiding exposure to loud sounds, bright light including sunlight, rapid jerky movements, bending at the waist, or twisting the head, all of which predispose to vertigo
• Encourage avoidance of nicotine, caffeine, and decongestants all of which have a vasoconstrictive effect
• Avoid fatigue and stress
• Use a white-noise machine to mask tinnitus PRN