asthma part 1 Flashcards
What is asthma
chronic inflammatory disorder of the airways in which many cells and cellular elements are involved
Risk factors for early (< 3 years of age) development of persistent astham
Has one of the following: parental history of asthma, history of atopic dermatitis, or evidence of sensitization to aeroallergens
Or
Has two of the following: evidence of sensitization to foods, >4% periphral blood eosinophilia, or wheezing not related to colds
Patient specific factors that predispose patients over 3 years to developing asthma
Genetic predisposition to development of asthma or atopy, gender ( more likely in boys younger than puberty and women over puberty), and obesity
Environmental factors that increase susceptibility to asthma
Biggest are allergens and occupational sensitizers
-Respiratory viral infections, allergens, industrial smog (sulfur dioxide), photochemical smog (ozone and nitrogen dioxide), diet, tobacco smoke, higher socioeconomic status, family size ( more likely if no siblings or just one), occupational stimuli
Asthma triggers
Biggest are allergens and respiratory viral infections (viral cause more severe causes)
- exercise is most common cause of brief triggers due to loss of heat, water, or both in the lungs
- emotions can make an attack worse but cannot cause an attack alone
- gastroesophageal reflux can trigger
- menstration can trigger
- freezing temps, high humidity, acute pollution can trigger
Drugs and preservatives that can trigger asthma
aspirin, NSAID’s, beta blockers can decrease effectiveness of beta agonists, benzalkonium chloride, sulfite preservatives
Structures of respiratory system
nose, nasal cavity, pharynx, larynx, trachea, bronchi and their smaller branches, and lungs
Structures of the trachea
also called wind pipe
- epithelium is ciliated pseudostratified columnar cells that propel debris-laden mucous toward pharynx, goblet cells are here as well and secrete mucous,
- mucousa contains elastic fibers to allow for flexibility during inspiration and recoil during expiration
- submucousa has serous and mucous glands
- outermost layer has C shaped cartilage rings for support, open end has trachealis muscles that when they contract they decrease diameter which helps expel stuff during coughing
What are the two zones of the respiratory tract and what are the main events that occur in them
Conducting zone: respiratory passages that conduct air between the atmosphere and the respiratory zone (bronchial tree is here, cartilage rings feed into sites of irregular cartilage plates, epithelium changes from a ciliated pseudostratified columnar cell type to a thinner epithelial cell, circular smooth muscle increase as conducting tubes get smaller)
respiratory zone: gas exchange between air and blood occurs here (terminal bronchioles feed into alveolar ducts)
Structure and function of the respiratory membrane
consists of a type I cell, a very thin basement membrane
and the capillary endothelial cell. Gas exchange occurs over this membrane.
Function of type 1 and type 2 cells
type 1 are alveolar epithelial cells and type 2 cover the alveolar surface epithelium and secrete pulmonary surfactant
Explain the function of the pleurae
thin, double walled serosa that separates that thoracic cavity and the lungs. Outer layer is parietal layer, visceral layer is the inner layer. Pleura cavity is in between the two layers and has intrapleural fluid to lubricate movement
How is atmospheric pressure, intrapulmonary pressure, and intrapleural pressure related to breathing
atmospheric pressure; pressure exerted by the weight of the air in the atmosphere surrounding the body (decreases as altitude increases)
intrapulmonary pressure; pressure within the alveoli (fluctuates with breathing phases)
intrapleural pressure; pressure in the pleural cavity ( this space stays negative between 4-6 mm Hg, if this pressure equalizes with Patm or Ppul then the lugs collapse)
What are the general steps of pulmonary ventilation and the roles of pressure and volume
Air flows to areas of less pressure so in inspiration Ppul pressure must decrease by increasing volume of lungs so that air will flow from Patm to Ppul. Then the reverse must happen for expiration
Describe inspiration
diaphragm and intercostal muscles contract, causing diaphragm to flatten and rib cage to open outwards to increase volume of lungs. Pip decreases to -6mm Hg compared to Patm, Ppul pressure drops as well allowing air to flow from Patm to Ppul until the pressure are equal. Accessory inspiration muscles can engaged to increase the volume of the lungs even more, these come into play during asthma
Describe expiration
normally is a passive process that depends on elastic recoil of the lungs. Inspiration muscles relax returning thoracic cavity and intercostal muscles to relaxing state, decreasing volume. Ppul rises to +1 mm Hg higher than Patm thus air flows from higher pressure in lungs to lower pressure in Patm
Discuss how these physical factors influence ventilation: airway resistance, alveolar surface tension, and lung compliance
Airway resistance: airflow is inversely proportional to resistance, conducting airways radius are the main determinant of resistance and they normally offer almost no resistance, ANS controls contraction of branchioles which increases resistance
alveolar surface tension: type 2 cells secrete surfactants to decrease the surface tension of the alveoli so they do not collapse
lung compliance: measure of how much change in lung volume results from a force that stretches it. Basically how much can the lunch stretch and recoil.Decreased surfactant can decrease compliance. Fibrosis (scar tissue) can also decrease complaince
Describe these lung volumes: tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume
tidal volume (tv): normal volume of air displaced during inhaltion and experation. during normal quiet breathing, about 500ml of air are inspired and about the same quantity is expelled for every breath
inspiratory reserve volume (IRV): amount of air that can be inspired over and above the normal resting TV.Max contraction of inspiratory muscles. Normally about 2100 to 3200mL
expiratory reserve volume (ERV):extra volume of air that can be expired after normal TV normally about 1000mL
Residual volume (RV): volume of air remaining in lungs after max expiration, about 1200mL
Define the following lung capacities: inspiratory capacity, functional residual capacity, vital capacity (forced vital capacity), and total lung capacity
inspiratory capacity(IC): max volume of air that can be inspired after a tidal expiration (TV+IRV)
functional residual capacity (FRC): volume of air remaining in the lungs after a TV expiration
Forced vital capacity (FVC): max amount of air that can be moved out after max inspiration (IRV+TV+ERV)
total lung capacity (TLC): max volume of air contained by lungs (FVC+RV)
What is dead space
the volume of air that stays in the conducting airways and never contributes to gas exchange, normally about 150ml
describe alveolar ventilation
the air that is exchanged between the atmosphere and the alveiolar taking into account the amount lost in dead space. Alveolar ventilation rate is frequency (breaths/min)x( tidal volume-dead space)
Describe the basic properties of gases including partial pressures, partial pressure gradients, and Henry’s Law, and explain how these properties impact gas movement in the body.
partial pressure: the amount of pressure exerted by a gas in the atmosphere is proportional to its % of the overall gas makeup of the atmosphere (N makes up 78.6% and the overall atmospheric pressure is 760 so N’s partial pressure is 78.6% of 760 mm Hg) In blood the higher the amount of the gas dissolved in the blood the higher the gasses partial pressure. partial pressure of gasses are different in the atmosphere than they are in the alveolar
partial pressure gradients: the differences in partial pressure between two systems.A partial pressure gradient exists between the alveolar air and pulmonary capillary blood and between systemic capillary blood and the tissue that they feed (helps drive what direction the gas will flow)
Henry’s law: when a gas is in contact with a liquid it will dissolve in proportion to its partial pressure. The temperature of the liquid also determines the solubility of the gas. (Henry’s law helps determine how much gas will dissolve into blood to be exchanged)
Describe pulmonary and capillary gas exchange in the tissues
pulmonary gas exchange moves CO2 out of the blood into the lungs and O2 out of the lungs into the blood ( gas moves based on its partial pressure gradient).capillary gas exchange moves O2 out of the blood into the tissues (the amount of O2 moved is proportional to the amount of work tissue is doing) and CO2 out of the tissues and into the blood.
What is the role of ventilation perfusion coupling
makes gas exchange more efficient by coupling or matching ventilation with perfusion. The two systems are never completely matched due to gravity or being plugged up. If an alveolar is having poor ventilation (low PO2) then the blood perfusion to that alveolar will be redirected to areas that have better ventilation, this is achieved by constricting arteries near poorly ventilated areas and dilating arteries in well ventilated areas.
If PCO2 changes then the diameter of the bronchioles are changed to allow for more rapid changes in PCO2, using constriction to allow for PCO2 to increase or dilation to allow more rapid elimination of CO2.
describe these neural systems that control respiration: medullary respiration centers, pontine respiratory centers, and respiratory rhythm
Medullary respiration center: Dorsal respiratory group (DRG), mostly inspiratory neurons, when these neurons fire inspiration occurs, when they stop inspiration stops. Ventral Respiratory Group (VRG), inspiratory and expiratory neurons, supplements the DRG, can be activated during periods of higher ventilation demands, play a role in active respiration, and during quiet breathing now impulses are needed here.
Pontine respiratory centers: fine tunes the medullary center so that inspiration and expiration are smooth, without this center regular breathing would be disrupted by periods of apneustic breathing
respiratory rhythm: it is believed that there are pacemaker cells like those in the heart that help with intrinsic rhythm
Describe the following factors that influence breathing depth and rate: carbon dioxide and oxygen levels, and arterial pH
Carbon dioxide: most potent and most closely controlled chemical that affects breathing, PCO2 is around 40 mm Hg, an increase causes pH to fall in the CSF which excites central chemoreceptors to cause increase is breathing depth and rate (hypercapnia). A decrease in PCO2 causes respiration to be inhibited and respiration becomes slow and shallow.
Oxygen:PO2 must change dramatically to cause an impact (drop to 60mm Hg) and increase ventilation
arterial pH:can adjust respiration when CO2 and O2 levels are normal, when pH decrease rate and depth of respiratory increase
what are the roles of cell-mediated and humoral immune responses in asthma
Early and late phase reaction. In early phase allergens bind IgE that is bound to mast cells thus releasing histamine, leukotrienes ( have a stronger affect on smooth muscle) also are synthesized and released, These steps induce contraction of airway smooth muscle, mucus secretion, and vasodilation. Bronchospasm can occur. Patients that only have the early phase will not have bronchial hyperresponsivness.
Late phase recruits eosinophils, basophils, neutraphils, and macrophags. TH2 cells are also matured, a lot like a normal late phase reaction. People who experience the late phase will have bronchial hyperresponsivness, can be for up to 6 weeks.
explain the role of bronchial epithelial cells, leukocytes, myofibroblasts, mast cells, and alveolar macrophages in asthma
bronchial epithelial cells:during asthma these cells are damaged which leads heightened airway responisvness, altered permeability of airway mucosa, loss of normal protectiveness
leukocytes: eosinophils are a rich source of leukotrienes like LTC4 which contract airway smooth muscle, increase vascular permeability, and recruit more eosinophils which also destroy local tissue. type 2 helper cells are also thought to play a role.
myofibroblasts: progenitor cells of muscle, they increase in number in asthma and contribute to inflammation, they also thicken the basement membrane
Mast cells and alveolar macrophages: cause inflammation, bring more cells in, and release things that destroy local tissue
describe the role of leukotrienes in asthma
Have a role in early and late phase. LTC4, LTD4, and LTE4 cause a prolonged contraction in the airway GI tract, they also promote inflammation
explain the following consequences to chronic inflammation: airway remodeling, mucous production, and airway smooth muscle growth
airway remodeling: can cause thickening of airways, once its chronically damaged it is replaced with connective tissue (scar tissue) which can lead to COPD
mucous production: mucous secreting cells in asthma are enlarged and increase in number, mucous plugs in airways are observed in asthma
airway smooth muscle growth: becomes hypertrophic, and hyperplasia occurs
