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148 Cards in this Set
- Front
- Back
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lung cancer = ___________ _________
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bronchogenic carcinoma
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cough, wheezing, dyspnea, hyperpnea, SOB, chest tightness, substernal retractions
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asthmatic symptoms
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treatment for asthma
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avoid triggers, meds before exercise, monitor ABGs, O2 supplement, maintainence therapy (corticosteroids, bronchodilators, leukotrienes, etc.)
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causes of COPD
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chronic lung irritation (from smoking, infx, inh irritants), genetic (ATT deficiency), aging (loss of elastic recoil of lung), socioeconomic factors
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assessment for COPD
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hx of smoking?, resp status? (note shallow resp, persistant cough, ineffective/adventitious breath sounds), eval. nutritional status
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relieve pain, improve resp status, improve nutritional status, promote biliary drainage and skin care, educ. and admin all meds, airway maintainence, O2 therapy are interventions for
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COPD
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education of cessation of smoking is the single most inportant intervention for:
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COPD
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complications of COPD include:
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hypoxemia and acidosis (acute resp failure = PaO2 50mmHg, PaCO2 50mmHg), resp infx, cardic failure (cor pulmonale)
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hypertrophy of the rt side of the heart with or w/out HF, resulting in pulmonary HTN and fluid retention
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cor pulmonale
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Tidal lung volume (TV)
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500mL
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total lung capacity (TLC)
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TV+IRV+ERV+RV=6000mL
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residual lung volume (RV)
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1200mL
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forced/functional vital capacity (lung) (FVC)
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amount of air that can forcibly be blown out after full inspiration ~5.0 L
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normal FEV1/FVC =
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80%
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Forced Expiratory Volume in 1 Second (FEV 1)
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amount of air forcibly blown out in one second ~ 4.0 L
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Flow Volume Loops in COPD
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FEV 1/ FVC ration < 80%; limiation of expiratory airflow
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Test for Normal Flow Volume Loop in Asthmatic patient
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Bronchoprovocation
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Drug used in bronchoprovocation
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methcholine: choline ester - rapidly metabolized by AchE
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contains 450 ml of total blood volume
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pulmonary arteries
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pulmonary artery pressure
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25/8
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gas exchange process
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passive diffusion of pressure gradient
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increase in temp (exercise), increased CO2/decreased pH, increased 2,3 DPG, acidosis causes...
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right shift dissociation curve of O2 (decrease in affinity)
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reduced dissociation of O2
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left shift
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catalyzer of RBC reaction of water and CO2
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carbonic anhydrase
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as HCO3- leaves RBC it is replaced by CL- causing
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Chloride shift
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Respiratory acidosis
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lungs do not ventilate properly and result in excessive CO2 in blood (incr. H+)
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Respiratory Alkalosis
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loss of H+ in blood and CSF; excessive loss of CO2 from body. Alkaline CSF inhibits repsiratory control center.
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competes with O2 for binding sites on Hgb, with an affinity that is 250 X that of O2
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CO (carbon monoxide)
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most common childhood chronic disorder
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asthma
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reversible pulmonary disorder: increased responsiveness of the bronchi to various stimuli (allergens)
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asthma
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irreversible pulmonary disorder
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COPD
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inflammation of bronchial walls, constriction of bronchial smooth muscle leading to reversible airflow obstruction (B2 R), incrased mucous secretion
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characteristic features of asthma
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predisposing factor for developing asthma
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atopy (incr. IgE levels due to environmental allergens)
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degree of airway obstruction/narrowing determind by
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diameter of airway lumen
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early-phase bronchospasm response
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release of inflammatory mediators from mast cells, macrophages, & epithelial cells (leukotriene, PG's, cytokines, etc)
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late/delayed inflammatory response
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mediators cause infiltration of airway walls w/eosinophils and neutrophils resulting in epithial injury & abnormal neural regulation of airway tone
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IL-3 and IL-5 increase ________ _________.
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eosinophil activation
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IgE induces growth of
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mast cells
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IL-4 stimulates ______ & increases producation of IgE.
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B-cells
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primary inflammatory mediator
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histamine
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secondary inflammatory mediators
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leukotrienes and prostaglandins
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adult-onset asthma
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Non-IgE induced due to nasal polyps, sinusitis, aspirin, NSAID sensitivity
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persistent asthma requires:
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"controller" pharmacological treatment
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Fast-acting relief of acute asthmatic symptoms
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short-acting beta-2 agonists (SABA)
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rescue med; SABA; relaxes airway smooth muscle and incr airflow in as little as 2-5 min
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Albuterol
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non-selective B1 & B2 agonist; emergency room med given in soln for inhalation (usually)
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epinephrine
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Gold standard SABA rescue inhaler
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albuterol
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B2-selective (3,5 substituted)agonist for COPD and bronchospasm; oral and inhalation
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metaproterenol
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B2-selective (3,5 substituted) for COPD, bronchospasm, status asthmaticus; oral, parenteral; tocolytic
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terbutaline
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adverse effects of fast-acting Beta bronchodilators, mostly mediated by B1 activity
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fine tremor!, tachycardia
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best treatment method for younger children or severe asthma episodes
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nebulizer
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important factors for deposition of inhaled drugs
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particle size (1-5 micrometers to be deposited in the lungs - not alveoli), rate of breathing, breath-holding after inhalation
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anticholinergics used in bronchodilation, best if used with B2 agonist
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ipratropium (Atrovent) and tiotropium (Spiriva)
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does not impede muccocillary clearance of mucous
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ipratropium
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MOA: suppresses cytosine production, airway eosinophilic recruitment, & other chemical mediators
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Inhaled corticosteroids (ICS)
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regulation of carbohydrate, protein, and lipid metabolism
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glucocorticoids
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oral glucocorticosteroids for severe asthma
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prednisone or prednisolone
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new generation synthetic glucocorticoid w/rapid metabolism by P4503A4 in liver which overcomes potential SE
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fluticasone
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more significant SE profile compared to inhaled steroids
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systemic steroids
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effect of long-term steroid use
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Iatrogenic Cushing's Syndrome
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requirement with dicontinuation of long term steroid therapy
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TAPER
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regulated cortisol
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ACTH
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inhibits CRH
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ACTH
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regulates ACTH secretion
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CRH
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inhibits ACTH
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cortisol
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hypercorticosteroids
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Cushing's syndrome
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hypocorticosteroids (rapid withdraw from steroid therapy)
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Addison's Syndrome => Addisonian crisis
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Long-acting B2 agonist; commonly used in combination with fluticasone (Advair)
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salmeterol (Serevent)
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NOT TOU BE USED AS RESCUE!
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salmeterol
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Long-acting B2 agonist: best for nocturnal asthma due to prolonged duration of action (up to 12 hrs)
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formoterol (Foradil)
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inhibit IgE-mediated release from mast cells; block Cl- channels in mast cells; modulate eosinophilic recruitment; inhibit bronchospasm
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Cromolyn & Nedocromil
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phosphodiasterase inhibitor => incr cAMP and bronchodilation; adenosine antagonist in bronchial smooth muscle
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theophylline (methylxanthines)
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narrow therapeutic index and incr SE profile - requires dose titration
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theophylline
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5-lipooxygenase inhibitor
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Zileuton (Zyflo CR)
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leukotriene R antagonists: inhibits CysLT1 R
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Zafirlukast (Accolate) & montelukast (Singulair)
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inhibits metabolism of theophylline and warfarin
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Zileuton (Zylfo CR)
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increases warfarin half-life & requires monitoring
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-lukasts
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____ are more effective at decreasing asthma exacerbations than anti-________ agents
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ICS; leukotriene
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combination therapy of ____ & _______ is better than increasing ICS dose alone
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ICS & Salmeterol
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a humanized MCA given SC that binds to and inhibits IgE in atopy
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Omalizumab (Xolair)
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forms complexes with free IgE, and inhibiting IgE binding to mast cell and basophils, decreasing mediator release, especially in patients with atopy
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omalizumab (Xolair)
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leukotriene inhibitors acts as ___________ & probable ___-_______ agents
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bronchodilators & anti-inflammatory
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inhaled bronchodilator; short-acting; 1st line for intermittent asthma
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albuterol
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1st line for any persistent asthma
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inhaled corticosteroids (fluticasone, budesonide)
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Step 1 approach to asthma tx (intermittent asthma)
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SABA PRN (albuterol)
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Step 2 approach to asthma tx persistent asthma (mild, moderate, severe)
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low-dose ICS or alternative (cromolyn, LTRA, theo); need to have SABA for rescue
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Step 3 approach to asthma tx
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low-dose ICS + long-acting B agonist (LABA) OR med-dose ICS OR + -lukast or zileuton
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Steps 4 thru 6 to asthma tx
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med to high dose ICS + LABA; no not controlled, + oral systemic steroids on reg schedula (lowest dose, and taper when controlled); consider Xolair w/severe allergies and incr. IgE
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medical emergency defined as failure of outpatient therapy
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status asthmaticus
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selective B1 & B2 agonist w/ positive inotropic and chronotropic effects
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isproterenol
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clinically defined by a low FEV1 value that fails to respond acutely to bronchodilators
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COPD
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produces significant systemic consequences
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COPD
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caused by chronic bronchitis or emphysema assoc. w/long-term tobacco smoking
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COPD
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persistent and progressive breathlessness; night time waking w/breathlessness &/or wheeze
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COPD
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main risk factor for COPD
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tobacco smoking
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mucous hypersecretion, ciliary dysfunction, pulmonary HTN, gas exchange abnormalities
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COPD patho changes
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chronic production of sputum & thickened bronchials w/ initial sxs of SOB, productive cough
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chronic bronchitis (symptoms greater than 3 mos)
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initial sxs: SOB and exertional dyspnea
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emphysema (destruction and distenstion of alveoli)
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"pink puffer"
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reddish complexion, puffing hyperventilation, large barrel-shaped chest (hyperinflation), prominent accessory muscles
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neutrophils & macrophages accumulate in ___________ in smokers
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alveoli
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neutrophils have _________ which are inhibited by a1-antitrypsin
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proteases
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thought to result from destructive effects of incr. protease activity in presence of decr. a1-AT activity
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emphysema
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breakdown of alveoli creating large sacs
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emphysema
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"blue bloaters"
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incr. secretions leading to hypoxia (cyanosis due to deoxygenated Hgb)
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pulmonary HTN
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results from cyanosis in chronic bronchitis (COPD); cor pulmonale (R ventricle dysfunction)
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respiratory failure, cor pulmonale, body compensates for hypoxemia w/incr. RBC = viscous blood (polycythemia)
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COPD complications
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FEV1/FVC in COPD pt
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</= to 70%
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four components of managing COPD
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assess/monitor disease; reduce RF; manage stable COPD (education, pharmacologic, non-pharmacologic); manage exacerbations
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primary objective of COPD management
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smoking cessation
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excessive mucous production obstruct airways
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COPD: Chronic Bronchitis
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initial therapy with ___________ drug for COPD
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anticholinergic
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cholinergic tone is the only reversible component of
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COPD
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drugs that decrease mucous hypersecretion
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anticholinergics
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2 antimuscarinics used for bronchospasm
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ipratropium & tiotropium
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selective for M1 and M3 R, long duration (24 hrs: once daily dosing)
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tiotropium (Spiriva)
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patients with moderate to severe sxs of COPD require
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combination of bronchodilators
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inhaled glucocorticoids only considered appropriate for symtomatic COPD patients with FEV1....
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<50%
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COPD Therapy Goals
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Prolong life & reduce sxs
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pulmonary infx & air pollution are most common causes of
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exacerbation
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contraindicated in stable COPD because cough is productive
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antitussives
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vaccines for prophylaxix of pulmonary infx
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influenza & pneumovax
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autosomal recessive inheritance (chromosome 7); multisystem disease
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Cystic Fibrosis (CF)
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cause of CF
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mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) on long arm of chromosome 7
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codes for a cAMP regulated Cl- channel
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CFTR
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most common lethal genetic disease in Caucasian populations
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CF
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increased mucous viscosity, decr. mucociliary action, mucus plugging, high rate of infx (psuedomonas)
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CF (LUNGS)
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accumulation of mucus in bile ducts leading to liver damage (hepatic cirrhosis); 2nd leading cause of death in this disease
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CF (LIVER)
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abnormally high BP in arties between heart and lungs
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Pulmonary HTN
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weakening of the lining of the lung's blood vessels results in leakage of blood
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pulmonary HTN
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Prostacyclin analogs for pulmonary HTN:
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Epoprostenol & treprostinil & iloprost
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decr. systemic & pulmonary vascular resistance; reduce dyspnea & fatigue in pulm HTN
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prostacyclin analogs
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endothelin (ET-1) antagonists
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bosentan
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phosphodiasterase inhibitors
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sildenafil
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derivative of naturally occring PGI-2, produces direct vasodilation of pulmoney and systemic arterial vascular beds, and inhibition of platlet aggregation
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epoprostenol (prostacyclin analog)
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stable synthetic prostacycomimetic drug that is substantially more stable chemically & metabolically than epoprostenol
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treprostinil & Iloprost(prostacyclin analogs)
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direct vasodilation of pulmonary and systemic arterial vascular beds
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treprostinil (& epoprostenol & iloprost)
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most potent vasoconstrictor that causes prolonged vasoconstriction and incr vascular tone, increasing PVR (mostly paracrine function)
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ET-1 (Endothelin-1)
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must be delivered into central venous circulation to achieve selective pulmonary vasodilation; T 1/2 ~ 6 min
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epoprostenol
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SC infusion usign a pump system; T 1/2 ~ 2-4 hrs
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treprostinil
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inhaled aerosol 6-9 times daily; Se of syncope due to systemic effects
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iloprost
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regulates intracellular level of cyclic quanosine monophosphate (cGMP)
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sildenafil
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diminishes the effect of PDE5, facilitates effect of NO, incr. cGMP, relaxes smooth muscle (vasodilates by relaxing arterial wall & incr pulmonary arterial resistance)
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sildenafil
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mediators of smooth muscle tone in pulmonary vasculature
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PGI2, ET-1, TXA2
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SE of Bosentan
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hepatotoxicity
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syncope, flushing, jaw pain SE of
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Iloprost
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flushing, nausea, diarrhea, jaw pain, HA SE of
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treprostinil
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toxicity = rebound pulmonary vasoconstriction, SE include dizziness, HA, jaw pain, thrombocytopenia, & sepsis
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epoprostenol
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SE include headache, nasal congestion, visual disturbance, CV events including HTN
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sildenafil
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