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32 Cards in this Set
- Front
- Back
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What is asthma according to the National Heart, Lung and Blood Institute?
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Asthma is a chronic inflammatory dz manifested by recurrent episodes of wheezing, breathlessness, chest tightness and coughing.
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What are the three key features about asthma that are essential to diagnosis, pathophys and treatment?
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- variable airflow obstruction that is reversible
- airway inflammation - increased bronchial or airway responsiveness to a variety of stimuli |
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Asthma is classified as [ obstructive / restrictive ] lung dz.
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Obstructive. It results in narrowing of airway lumen, a slowing of air flow, and increased resistance to air flow.
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Airflow obstruction is best demonstrated by characteristic changes in pulmonary function. With regards to spirometry, how does asthma affect:
A. FEV1 B. FEV1/FVC C. PEFR (peak expiratory flow rate) D. expiratory time |
A. FEV1 - decreases
B. FEV1/FVC - decreases (due to decreased FEV1) C. PEFR (peak expiratory flow rate) - decreases D. expiratory time - increases |
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As asthma is an obstructive dz, what are characteristics of obstruction with regards to:
A. residual volume (RV) B. FRC (functional residual capacity) C. TLC (total lung capacity) D. compliance ( shift left or right?) |
A. residual volume (RV) - residual volume increases
B. FRC (functional residual capacity) - this increases since this includes RV C. TLC (total lung capacity) - this increases since this includes RV D. compliance ( shift left or right?) - compliance increases since there is loss of elasticity. This manifests as a left shift in the compliance chest lung curve (higher FRC) |
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With asthma, airflow obstruction is either partially or completely reversible. This is in contrast to someone with what other respiratory condition?
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COPD
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Signs and symptoms of asthma may not develop until there is a _____% decline in FEV1.
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30-50%
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In asthma, airflow obstruction occurs due to various things. Elaborate how each of the following contributes to airflow obstruction.
A. acute bronchochonstriction B. Cellular changes C. Cellular edema D. Mucus E. Airway remodeling |
A. acute bronchochonstriction - smooth muscle contraction and hypertrophy.
B. Cellular changes - eosinophil and lymphocyte infiltration and activation mast cell activation C. Cellular edema - increased microvasc permeability --> leakage results in mucosal thickening and airway swelling which leads to airflow limitation, even in absence of smooth muscle contraction D. Mucus - chronic mucus plug formation occurs E. Airway remodeling - potentially permanent changes in architecture of the airway and surrounding extracellular matrix |
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Asthma is characterized by exaggerated bronchoconstrictor response to a variety of stimuli. Bronchial hyperresponsiveness refers to the fact that asthmatic airways have propensity to narrow too easily and too much in response to stimuli which would cause little or no physiologic change in normal airways. How is bronchial hyperresponsiveness quantified?
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By identifying the amount of histamine or methacholine required to induce a 20% fall in FEV1. This amount is called the methacholine (or histamine) PC20.
Note BHR is not a fixed characteristic but rather changes with time and reflects the severity of the dz and presence of symptoms more so than resting lung function. |
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Regarding the cells and mediators of asthma pathogenesis, this is one of the characteristic cells of asthma. It is found in increased numbers in airways in response to allergen challenge and can also be found mildly increased in numbers in blood. Releases factors that include cationic proteins which are toxic to epithelium and cause degranulation of basophils and mast cells. Lipid mediators such as LTC4 and platelet activating factors are also released by this mediator.
A. Eosinphils B. Lymphocytes C. Macrophages D. Mast cells |
A. Eosinphils
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Regarding the cells and mediators of asthma pathogenesis, this
- is not necessarily found in increased numbers, but rather in an increased state of activation. - releases both preformed mediators like histamine and eosinphil chemotactic factor - newly generated mediators like leukotrienes which --> bronchoconstriction, increased permeability and edema formation, promotion of mucus secretion and eosinophil chomattractant - newly generated cytokines like IL-4, IL-5 and TNF-alpha A. Eosinphils B. Lymphocytes C. Macrophages D. Mast cells |
D. Mast cells
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Regarding the cells and mediators of asthma pathogenesis, mast cells are responsible for releasing both preformed and newly generated mediators and cytokines. What are the four effects of leukotriene release in airways?
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Mast cells release newly generated mediators leukotrienes which have the effects of:
- bronchoconstriction - increased permeability and edema formation - promotion of mucus secretion - eosinphil chemoattractant |
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Regarding the cells and mediators of asthma pathogenesis, mast cells release newly generated cytokines IL-4, IL-5 and TNF-alpha. Which is described below:
promotes growth and activation of B cells as well as stimulating them to swithc production of IgM to IgE |
IL-4
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Regarding the cells and mediators of asthma pathogenesis, mast cells release newly generated cytokines IL-4, IL-5 and TNF-alpha. Which is described below:
eosinophil maturation, release, activation and survival |
IL-5
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Regarding the cells and mediators of asthma pathogenesis, mast cells release newly generated cytokines IL-4, IL-5 and TNF-alpha. Which is described below:
proinflammatory cytokine involved in virtually all inflammatory processes. Needed for vascular endothelium to express adhesion molecules. |
TNF-alpha
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Regarding the cells and mediators of asthma pathogenesis, this
- is the most common inflammatory cell in the normal airway - found in increased numbers AND increased state of activation in asthmatics, especially after an allergen challenge - help mediate allergic inflammation by amplifying growth, activity and or longevity of eosinophils and mast cells A. Eosinphils B. Lymphocytes C. Macrophages D. Mast cells |
B. Lymphocytes
also: - are specifically CD4 (T-helpers) which produce Th2 type cytokines (IL-4,5,6,9,13) that mediate allergic inflammation by amplifying growth, activity and or longevity of eosinophils and mast cells |
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Regarding the cells and mediators of asthma pathogenesis, this
- is found in both airways and alveoli - processes foreign antigen to present to lymphocytes - while they can release mediators such as PAF, thromboxane and prostaglandins, their role in asthma is less clear A. Eosinphils B. Lymphocytes C. Macrophages D. Mast cells |
C. Macrophages
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Some neuropeptides (Neurokinin, Substance P, Vasoactive intestinal peptide) might also be a cause of asthmatic dz. Match em with their description.
1. normally a potent relaxant of airways. Is degraded more quickly in asthma, leading to exaggerated bronchoconstrictor responses 2. potent inducer of mucus secretion and microvascular permeability 3. potent bronchoconstrictor |
1. normally a potent relaxant of airways. Is degraded more quickly in asthma, leading to exaggerated bronchoconstrictor responses- VASOACTIVE INTESTINAL PEPTIDE
2. potent inducer of mucus secretion and microvascular permeability - SUBSTANCE P 3. potent bronchoconstrictor - NEUROKININ |
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Some neuropeptides (Neurokinin, Substance P, Vasoactive intestinal peptide) might also be a cause of asthmatic dz. Which is normally a potent relaxant of airways. Is degraded more quickly in asthma, leading to exaggerated bronchoconstrictor responses.
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Vasoactive intestinal peptide.
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Some neuropeptides (Neurokinin, Substance P, Vasoactive intestinal peptide) might also be a cause of asthmatic dz. Which is a potent inducer of mucus secretion and microvascular permeability?
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Substance P
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Some neuropeptides (Neurokinin, Substance P, Vasoactive intestinal peptide) might also be a cause of asthmatic dz. Which is a potent bronchoconstrictor
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neurokinin
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The airway reaction in asthma attacks can be divided into two distinct events: early and late asthmatic responses. In the early asthmatic response,
A. onset is in how many minutes? when does it subside? B. what airway obstructive mechanism does it involve? C. what are potential triggers D. how can it be pharmaceutically staved off? E. does it affect BHR? |
In the EARLY asthmatic response:
A. onset is in 10-15 minutes, subsides in an hour B. what airway obstructive mechanism does it involve: is a purely bronchospastic event (primarily due to smooth muscle contraction) C. potential triggers: allergens, exercise, cold air, hyperventilation, irritants like smoke, dust and fumes, drugs. D. how can it be pharmaceutically staved off: beta 2 agonists and sodium cromoglycate inhibit this bronchospastic response E. does it affect BHR: NO, it does not (onlythe late asthmatic repsonse leads to increase in BHR, which can last for several days) |
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The airway reaction in asthma attacks can be divided into two distinct events: early and late asthmatic responses. In the late asthmatic response,
A. onset is in how many minutes? when does it subside? B. what airway obstructive mechanism does it involve? C. what are potential triggers D. how can it be pharmaceutically staved off? E. does it affect BHR? |
A. onset is in 5-8 HOURS after challenge and may last 24 hours or more
B. what airway obstructive mechanism does it involve: airway narrowing due to inflammation, edema, mucus hypersecretion combined with smooth muscle narrowing C. triggers: allergens, viral infections, ozone D. how can it be pharmaceutically staved off: corticosteroids and sodium cromoglycate prevents the late response E. does it affect BHR : YES, it increases BHR, which may last for several days. |
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True or False:
Gastroesophageal reflux can trigger asthma. |
TRUE. Is one of the miscellaneous factors listed as able to trigger asthma. Other misc factors are: weather, stress, irritant odors or fumes.
Non-misc: air pollution, sulfur dioxide, ALLERGENS, exercise, hyperventilation, cold dry air, infections |
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What are the symptoms of asthma that a patient might describe? (4)
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chest tightness, cough, wheezing, dyspnea
patient may experience all, some or non between attacks.. Onset may be slow or rapid, and might not be able to id cause or trigger. Frequency of occurrence is variable. Clinical SIGNS of asthma: tachypnea, wheezing, prolonged expiratory phase, cough, accessory muscle use |
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Regarding laboratory evaluation of asthma, routine biochem and hematology values should all be normal except for mild ______ in 30-50% of patients.
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eosinophilia
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Chest xray findings can be normal or can show __________ in asthmatics.
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hyperinflation, atelectasis from mucus plugging.
Mostly the xray is helpful in ruling otu other pulmonary dz or complications such as pneumonia, pneumothorax, or heart failure |
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Arterial blood gases are typically mildly low with asthma (low PaO2, PCO2). Why?
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- abnormal distribution of both pulmonary blood flow and ventilation due to unequal airflow obstruction adn mucus plugging which results in abnormal V/Q relationships and arterial hypoxemia
- reduced PCO2 less well understood, but chemoreceptors and carotid bodies seem to play role in hyperventilation seen - severe airflow obstructionadn possibly impending respiratory failure suggested by more significant decreases in PaO2, normal or increasing levels fo PCO2 and the presence of lactic acidosis |
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Not all that wheezes is asthma. What else is included in a differential diagnosis of wheezing?
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Asthma, COPD, heart failure, pulmonary embolism, upperairway obstruction, foreign body aspiration, acute bronchiolitis (in kids).
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_______, while not the sole cause of asthma, remains an important initiating event.
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Allergies
other causes: exercise, hyperventilation of cold, dry air, infections especially viral ones |
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Quick relief of asthma attacks are provided by short-acting ____ agonists.
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beta2
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Regarding the pathology of asthma, what are the gross and micro changes? (3)
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Inflammation, bronchospasm, hypersecretion of mucus
Additionally, in bronchial asthma, grossly you can see hyperinflated lungs, patchy ateclatasis, and thick mucus in bronchi. There is goblet cell hyperplasia, thickened basement membrane, inflammation and hyperplastic smooth muscle adn mucus glands |
