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| Question | Answer |
| Name 2 OBSTRUCTIVE AIRWAY DISEASES | Asthma Congestive Obstructive Pulmonary Disease (COPD) |
| What is the purpose of the RESPIRATORY SYSTEM? | is to provide a place of OXYGEN and CARBON DIOXIDE exchange between air and blood. |
| VENTILATION is the movement of air from where to where? | from the atmosphere into and out of the lungs air is taken in from the upper airway passages (nasal, nose, mouth, larynx and pharynx) Air then moves to lower airway (trachea, bronchi and bronchioles) |
| What is PERFUSION? | movement of BLOOD through the LUNGS |
| What is DIFFUSION | is the movement of GASES between the ALVEOLI and the capillaries that supply the alveoli. |
| Does asthma have its onset in childhood/adolescence or adulthood? | usually in childhood/adolescences, however adults can still develop it without a previous history of the diseases. it arises from a complex interaction between hereditary and environmental factors and manifests as acute attacks. |
| List the manifestations of Asthma | it is a chronic reactive airway disorder characterize by resistance to airflow due to episodic airway obstruction. Inflammation of the airways bronchospasm Increased mucous secretion and injury to mucosal lining of the airways |
| Asthma can be characterized as EXTRINSIC or INTRINSIC. Define each and what causes them. | EXTRINSIC aka ATOPIC: an allergic reaction initiated by a type 1 hypersensitivity response to an extrinsic antigen. INTRINSIC aka NON-ATOPIC: initiated by diverse non-immune mechanisms. Triggered by IRRITANT receptors and vagal reflex. Also by viral infections, inhaled irritants, NSAIDS and emotional stress. |
| EARLY phase or ACUTE response to asthma, when does it occur? | occurs within 10-20 min of exposure to trigger and can last up to 2 hrs (allergen binds to preformed IgE [type of antibody] on sensitized MAST CELLS found in the mucosal surface of airways. Mast cell activation releasing inflammatory mediators, causing MAST CELL DEGRANULATION) |
| in the ACUTE phase of asthma, direct stimulation of PARASYMPATHETIC receptors causes what? | BRONCHOSPASM & increased VASCULAR PERMEABILITY which causes MUCOSAL EDEMA & increased MUCOUS SECRETIONS |
| when does LATE PHASE response occur and how long does it last? | 4-8 hours after exposure to a trigger and may persist for days or even weeks |
| Late Phase response involves what? | inflammation, increased airway, responsiveness and renewed bronchospasm. these symptoms lead to further airflow limitation and continued heightened airway responsiveness. |
| treatment for all asthma pt's is approached in what two ways? | 1. control of factors contributing to asthmas severity 2. pharmacologic treatment (corticosteroids, bronchodilators, mast cell stabilizers, beta-AGONISTs, anticholinergic drugs) |
| Evaluation of asthma includes what 4 things? | 1. Assessment findings 2. Laboratory results 3. Radiological findings 4. pulmonary function tests 5. peak flow measurement |
| Prevalence of Asthma - who is it highest in? | off-reserve Aboriginal people 12 yrs and over. As well as a higher prevalence in boys and women. |
| Is the prevalence of asthma increasing or decreasing? what about prevalence of asthma attacks? What about asthma mortality rates? | Prevalence of asthma is increasing. Attacks are decreasing mortality rates are decreasing |
| When is childhood asthma susceptibility determined in life? | During fetal development and the first 3-5 years |
| List the 4 risk factors for developing childhood asthma | 1. family hx of allergy and allergic disorders incl hay fever, asthma and eczema 2. High exposure of susceptible children to airborne allergens 3. exposure to tobacco smoke in utero or early in life 4. low birth weight and respiratory distress syndrome |
| In the US is asthma higher in urban nor rural areas? | urban |
| List the 2 main risk factors for adult onset asthma and the 3 main ones for women | 1. Occupational exposure to low molecular weight sensitizers (chemicals people have allergic reactions to) 2. exposure to infectious agents, allergens or pollution 3. for Women - smoking, obesity, hormonal influences |
| the etiology of asthma is multi-modal and most often without one singular cause. True or false? | True |
| Asthma is characterized by... | Sudden recurrence or persistent symptoms such as DYSPNEA, CHEST TIGHTNESS, WHEEZING, SPUTUM PRODUCTION and COUGH associated with variable AIRFLOW LIMITATION and airway HYPERRESPONSIVENESS to stimuli. |
| What are the main mechanisms (natural process by which something takes place or is brought about) leading to the development and persistence of asthma? | Inflammation and its resultant effects on airway structure. |
| Are the symptoms of asthma the same in all patients? | No - it can vary greatly from one patient to another and symptoms may be transient, intermittent or persistent. |
| In asthma is the lower airway obstruction usually reversible? | Yes in asthma (in COPD it is not) |
| What are the triggers for EXTRINSIC aka ATOPIC or ALLERGY ASTHMA | a TYPE 1 IgE mediated Hypersensitivity reaction - resulting from exposure to an EXTRINSIC ANTIGEN/ALLERGEN |
| What are the triggers for INTRINSIC or NON- ATOPIC asthma | *viral rest tract infections, exercise, hyperventilation, cold air, weather changes, exercise, drugs and chemicals, irritants, hormonal changes & emotional upset, airborne pollutants, GERD |
| Do most individuals with asthma have extrinsic or intrinsic asthma? What is the major pathologic feature of both types? | most have a combination of extrinsic and intrinsic. Major Pathologic feature of intrinsic and extrinsic asthma is INFLAMMATION that results in HYPER RESPONSIVENESS of the AIRWAYS |
| During the early phase response, Mast cell activation releasing ____ mediators increase MUCUS secretion, increase VASCULAR PERMEABILITY and BRONCHOCONSTRICTION | INFLAMMATORY MEDIATORS - histamine, chemotactic chemokine, leukotrienes, prostaglandin D2, cytokines, platelet activating factor |
| Late Phase Response: release of INFLAMMATORY mediators causes recruitment of INFLAMMATORY CELLS which cause what to happen? | cause EPITHELIAL INJURY & EDEMA, INCREASED MUCUS, changes in mucociliary function resulting in the ACCUMULATION of MUCUS and increased AIRWAY RESPONSIVENESS (airway narrowing) & BRONCHOSPASM |
| List the INFLAMMATORY MEDIATORS/CELLS involved in the inflammatory process and in the pathogenesis (development of the disease) of asthma | MAST CELLS - degranulate releasing: Histamine, Chemotactic factor & Cytokines Mediators: Platelet activating factor (PAF), Leukotrienes, Prostaglandin D2, also cytokines & growth factor (long term response) T lymphocytes (TH2=T helper 2) Leukocytes |
| HISTAMINES role in asthma | causes SMOOTH MUSCLE to CONTRACT causing BRONCHOCONSTRICTION when stimulated in the bronchi Vasodilator causing increased vascular permeability through retraction of endothelial cells |
| LEUKOTRINES role in asthma | similar and complementary to histamine more potent and stimulate slower and more prolonged effects Slow and Sustained CONSTRICTION of the bronchioles |
| Prostaglandin D2 role in asthma | causes vasodilation, increased vascular permeability and bronchoconstriction |
| CHEMOTACTIC CHEMOKINES role in asthma | are cytokines that ATTRACT immune and INFLAMMATORY CELLS (primarily leukocytes) |
| CYTOKINES (TNF-alpha, IL-4, IL-5) role in asthma | defined as proteins that modulate the function of other cells |
| PAF (platelet activating factor) role in asthma | causes bronchospasm, eosinophil infiltration and non-specific bronchial hyper-reactivity |
| T LYMPHOCYTES (T helper 2), do they play an important role in INTRINSIC or EXTRINSIC | EXTRINSIC |
| Bronchospasm is | a sudden constriction of the muscles in the walls of the bronchioles. It is caused by the release (degranulation) of substances from mast cells or basophils under the influence of anaphylatoxins. It causes difficulty in breathing which can be very mild to severe. |
| During a bronchospasm, is the parasympathetic (rest and digest) control of the airway functioning properly? | No - it is not functioning appropriately due to heightened responsiveness to cholinergic editors. An increase in acetylcholine causes bronchial smooth muscle contraction and further mucus secretion. |
| MUCUS HYPERSECRETION is a major pathophysiological feature of asthma. How does it work? | SUBMUCOSAL glands and GOBLET cells produce mucus in the airways resulting in Goblet Cell Hyperplasia (enlargement ) & Submucosal Gland Hypertrophy (also enlargement). Mucus secretion is triggered by the inflammatory response. |
| LEUKOTRIENES are known to stimulate what? INTERLEUKIN-9 & 13 are the 2 most relevant cytokines that up-regulat what? | Mucus production. Mucus secretion |
| What is the most damaging effect of MUCUS HYPERSECRETION? | airway obstruction by mucus plugs Mucus hypersecreation may also increase airway HYPER-RESPONSIVENESS |
| What is this the definition of? increase in goblet cells, hyperplasia & hypertrophy of smooth muscle cells, leading to a thickened smooth muscle layer, inc airway deposition of collagen & other proteins resulting in thickening of the lamina reticular with sub epithelial fibrosis & inc vascularity in the airway wall. | AIRWAY REMODELING |
| AIRWAY REMODELLING : structural changes in the airway wall probably occur in parallel with ____ | INFLAMMATION meaning the more inflammation equals more airway remodelling. airway remodelling begins early on in the disease process of asthma and declining lung function |
| WRITE OUT IN COLOUR THE PUTTING IT ALL TOGETHER PAGE 14 | WRITE OUT IN COLOUR THE PUTTING IT ALL TOGETHER PAGE 14 |
| explain the IMMEDIATE or EARLY PHASE | response is TRIGGERED by activation of PRE-SENSITIZED IgE-COATED MAST CELLS Mast Cell DEGRANULATION results in the release of INFLAMMATORY MEDIATORS that increase mucus production, open mucosal intercellular junctions with exposure of submucosal mast cells to the ANTIGEN and cause BRONCHOSPASM |
| explain the LATE_PHASE | response involves the release of other INFLAMMATORY MEDIATORS, recruitment of NEUTROPHILS, EOSINOPHILS & BASOPHILS; increased vascular permeability, epithelial cell injury with DEC MUCOCILIARY FUNCTION & INC AIRWAY RESPONSIVENESS & BRONCHOSPASM |
| WRITE OUT CLINICAL MANIFESTATIONS ON PAGE 17 | WRITE OUT CLINICAL MANIFESTATIONS ON PAGE 17L |
| SYMPTOMS of asthma are subjective in nature and are reported by the patient. They may include | DYSPNEA or SOB CHEST TIGHTNESS COUGH (increased sputum) WHEEZING |
| DYSPNEA | result of an inability to adequately ventilate and abnormal ventilation perfusion relationship where parts of the lung that are well perfused aren to adequately ventilated |
| CHEST TIGHTNESS | results from air trapping and resultant hyperinflation of the lungs |
| COUGH | results as the asthmatic patient tries to clear his or her airway of mucus. In the absence of infection, the cough will initially be non-productive during an asthma attack |
| WHEEZING | is the result of the passing of air through narrowed airways. Initially, wheezing will be expiratory as the obstruction is in the lower airways. |
| If AIRWAY OBSTRUCTION PERSISTS what can happen? | Worsening HYPOXEMIA and RETENTION of CARBON DIOXIDE with associated RESPIRATORY ACIDOSIS (increased CO2 decreases blood pH), resulting in respiratory failure. |
| What are some of the signs you may notice upon inspection of a person with asthma? | Increased work breathing Use of accessory muscles Prolonged expiration Wheezing Cough & an inability to maintain a conversation |
| Upon AUSCULTATION what might you notice with a patient who has asthma? | Wheezing Distant breath sounds other Adventitious breath sounds such as Crackles (related to infection) * quiet or distant breath sounds mean that air is not moving |
| Vital Signs of someone with Asthma | TACHYPNEA (abnormally rapid breathing) TACHYCARDIA (abnormally rapid HR) DEC O2 SATURATION (hypoxemia) |
| explain why someone with asthma may be TACHYCARDIC | may be the result of anxiety, stress and or the use of quick relief meds like Ventolin |
| What is the most helpful Lab Value in asthmatic patient? | ABG (arterial blood gas) - provides info about ventilation through the pCO2 and PO2 values. |
| Hyperventilation will INITIALLY cause respiratory ALKALOSIS which may be accompanied with hypoxemia or a low pO2 during an attack BUT with persistent worsening the patient will progress to what? | respiratory ACIDOSIS due to HYPERCAPNIA or RETENTION of CO2 |
| how can the acid-imbalances and hypoxemia associated with asthma be addressed? | With OXYGEN administration and pharmacologic therapy to open airways and improve ventilation. Mechanical ventilation & critical care management is required for severe RESPIRATORY ACIDOSIS & HYPOXEMIA |
| What does a high pH of 7.50 indicate? What does a low pO2 of 76 indicate? | RESPIRATORY ALKALOSIS HYPOXEMIA |
| What does a low pH of 7.35 indicate? What does a high pCO2 of 49 indicate? What does low pO2 of 70 indicate? | RESPIRATORY ACIDOSIS HYPOXEMIA |
| what are the normal ABG values? pH pCO2 HCO3 pO2 | pH 7.35-7.45 pCO2 35-45 HCO3 22-26 pO2 80-100 |
| What are the various tests commonly done as part of the work-up for a patient in respiratory distress? | Physical assessment Labs (ABG's) Radiological findings (chest x-rays) Pulmonary function tests peak flow monitoring |
| Chest x-rays - what are the common radiological findings for an asthmatic patient experiencing an acute exacerbation of the disease. | HYPERINFLATION +/- FLATTENING of the semi-diaphragms respiratory INFECTION if there is one |
| which is the more common trigger of an exasperation of asthma, a viral or bacterial respiratory infection? Are antibiotics warranted? | VIRAL antibiotics are not warranted for viral infections |
| What is the most OBJECTIVE MEASUREMENT of LUNG FUNCTION? | Pulmonary function test using SPIROMETRY May be used in the initial diagnosis, monitoring ongoing response to therapy, assessing airway function & to validate peak flow monitoring. |
| List the 3 Pulmonary Function Tests | 1. SPIROMETRY (most objective) 2. BRONCHIAL PROVOCATION - using histamine, methacholine or non-pharmacologic agent (i.e. cold air) 3. Bronchial RESPONSIVENESS & bronchial OBSTRUCTION s/b REVERSIBLE following administration of short-acting BRONCHODILATOR (B2 agonist) |
| How is PEAK FLOW MONITORING used? | measures the Peak Expiratory Flow or how quickly a person can exhale. It can be done at home comparing the results to patients personal best. around same time each day, using best of three readings |
| PEF > 80% of personal best indicates? PEF 50-80% indicates? PEF < 50% indicates? | person is in GREEN zone, asthma is WELL CONTROLLED person is in YELLOW zone, CAUTION - use short acting bronchodilator and repeat PEF person is in RED zone, MEDICAL ALERT - take short acting bronchodilator & seek MEDICAL ATTENTION |
| Medication for asthma can be separated into 2 categories: LONG-TERM control and QUICK -RELIEF medications. What do each address? | LONG-TERM: addresses inflammation and airway obstruction QUICK-RELIF: reverses acute airflow obstruction |
| List 3 classes of Quick-Relief medications for asthma | 1. BETA 2 AGONIST (Bronchodilator) 2. ANTICHOLINGERGIC (Bronchodilator) 3.SYSTEMIC CORTICOSTEROIDS |
| how does a BETA 2 AGONIST (quick relief) work? *can affect Beta 1 receptors in the heart, causing TACHYCARDIA | i.e. Salbutamol - act on Beta 2 (1 heart, 2 lungs) pulmonary receptors inc levels of cyclic adenosine monophosphate (cAMP) and relaxing smooth muscle which results in BRONCHODILATION |
| how does an ANTICHOLINERGIC (quick relief) work? | i.e. Ipratropium - inhibits MUSCARINIC CHOLINERGIC receptors, reducing Vagal tone of the airways which results in BRONCHODILATION |
| how does a SYSTEMIC CORTICOSTEROID (quick relief) work? | these are sometimes used in SEVER asthma EXACERBATIONS. they block the CYCLOOXYRGENASE & LIPOXYGENASE pathways in the in INFLAMMATORY PROCESS. |
| What are 3 classes of LONG-TERM CONTROL Medications? | 1. LONG-ACTING BETA 2 AGONIST 2. MAST CELL STABILIZERS 3. MONOCLONAL ANTIBODY |
| How does a LONG-ACTING BETA 2 AGONIST work? **** cAMP *** | function in the same way as short-acting beta 2 agonist meds but last longer act on Beta 2 (1 heart, 2 lungs) pulmonary receptors inc levels of cyclic adenosine monophosphate (cAMP) and relaxing smooth muscle which results in BRONCHODILATION |
| how does a MAST CELL STABILIZER (long-term control) work? | stabilize the membrane of a sensitized mast cell after an ANTIGEN-IgE interaction, preventing the release of inflammatory mediators such as histamine. |
| how does the MONOCLONAL ANTIBODY subcutaneous injection (long-term control ) work? | is an anti-IgE antibody that prevents the binding of IgE to basophils and mast cells. |
| which is the preferred quick relief medication? | BETA 2 AGONIST inhalations with ANTICHOLINERGIC medication as adjuvant therapy |
| What should be included in patient teaching for a pt with asthma? | Avoid triggers and recognize signs of impending attack written plan for meds & symptom management use peak flow monitoring medication adherence proper inhaler technique, delivery device |
| Is the prevalence of asthma increasing in Canada and worldwide or decreasing? | INCREASING |
| Pharmacologic interventions are aimed at decreasing ____ and addressing ____ | decreasing inflammation and addressing bronchoconstriction |
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