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230 Cards in this Set
- Front
- Back
Where does the respiratory system begin?
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The nose
|
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What is the role of the nose in preventing foreign particles from entering the body?
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The nose has coarse hairs to trap insects and large particles to prevent them from entering the inner tracts
|
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What system lines the airwarys of the respiratory tract?
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The mucocilliary system
|
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What does the mucocilliary system consist of?
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Fine cillia that are able to carry foreign particles trapped in the mucus to the larynx where it can be disposed to the stomach
|
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What does the trachea divide into?
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The bronchi in the right and left lungs
|
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What do bronchi divide into?
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Smaller bronchioles
|
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What do bronchioles eventually end in?
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Alveoli
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How are alveoli important?
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They significantly increase the surface area of the lung where gas exchange can occur
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How can analysis of the thorax determine if one has a respiratory disease?
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One can use X-ray to see if the shapes of the organs (lungs, bronchi, heart and diaphragm) are abnormal
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What can the lung be divided into?
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Lobes
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How many lobes are in the right lung?
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Three
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How many lobes are in the left lung?
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Two
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What can the lobes of the lung be divided into?
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Bronchopulmonary segments
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What are these bronchopulmonary segments based on?
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The branching of the smaller brochioles
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How many bronchopulmonary segments does the right lung have?
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10
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How many bronchopulmonary segments does the left lung have?
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8
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Why is this compartment of the lung into bronchopulmonary segments useful?
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It is a good asset when you want to remove part of the lung
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Why is this beneficial when you want to remove part of the lung?
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Each bronchopulmonary segment has only one connection to the main bronchi branches
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Which segments are more susceptible to disease or damage?
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If the tracts leading to that segment are more in line with the trachea than foreign particles are more likely to fall there
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Why can someone function even when removing up to a whole lung?
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The total surface area of the lungs are huge and allow for alot of gas exchange
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What is characteristic about the airways in the distal regions of the lung?
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The airways are smaller and lined with various cells
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What types of cells are these small airways lined with?
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Ciliated epithelial cells and Clara cells
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What are Clara cells?
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Non-cilliated epithelial cells
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How many cillia does each cilliated cell typically have?
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~200
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At what rate do cillia typically beat?
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6 Hz
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What do distal airways secrete?
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Surfactant
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What is the role of surfactant?
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The stability of airways
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What is surfactant produced by?
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Type II pneumocytes in the epithelial lining of the alveoli
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Where does gas exchange take place?
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Between the epithelial cells lining the alveoli and the endothelium of the pulmonary circulation in the basement membrane
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What lines the airways?
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Cilliated and non-cilliated epithelium
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What are Goblet cells?
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Part of the epithelial lining, non-cilliated cells that are responsible for the production of mucus
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At what point in the airway do the cilia have the greatest frequency of movement?
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In the larger areas, such as the trachea, there is an increased frequency of movement
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What type of cells are underneath the epithelia?
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Inflammatory cells, such as macrophages, which are part of the lungs defence system
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In the bronchioles and large airway, what is underneath the epithelium?
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A layer ofmuscle
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What is the embryological origin of the respiratory system?
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The fore-gut
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What did the fore-gut seperate into?
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The trachea and esophagus
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Where does cartilage exist around the smooth muscle of the airways?
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Only in the larger airways (NOT the bronchioles)
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What is the role of cartilage that surrounds the airways?
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It holds them open
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What is the role of the macrophages in the alveoli?
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To remove any foreign particles that were not caught and transported by the mucociliary system
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What is the role of the hair and cilia in the nasal cavity?
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To trap particles and expel them
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Where can the hair and cilia in the nasal cavity expel the foreign particles?
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Out into the external environment or to the stomach
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What protection do the proximal airways have?
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The mucociliary transport system
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What additional protection do the distal airways (alveoli etc) have?
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Macrophages continually engulph foreign particles and will also ge transported by the mucociliary transport system after they have exhausted their phagocytic ability
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What is under the epithelial layer of the airways that is unique to the respiratory system?
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A system of lymphoid tissue
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What is the main immunoglobulin produced in this special lymphoid tissue under the epithelial layer?
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IgA
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What is this IgA secreted by?
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Local plasma cells in the lymphoid tissue
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Where are the IgA secreted?
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Onto the surface of the epithelial lining
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What is the function of IgA on the epithelial surface?
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They act in the mucus to prevent pathogen infection, where they are removed by the mucocilliary transport
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Which organ is the epithelial lining of the lung similar to?
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THe kidney
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Where are lymphatics located in the lung in addition to underneat the epithelia of the airways?
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The pleura of the lung
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What is a viral infectionof the nose?
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Rhinitis
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What is a viral infection of the nose called?
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The cold
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What are some symptoms of the cold?
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Nasal obstruction, nasal discharge
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What is a viral infection of the pharynx?
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Pharyngitis
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What are some symptoms of pharyngitis?
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Sore, red throat that may be accompanied by exudate
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What is viral infection of the larynx?
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Laryngitis
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What are some symptoms of layrngitis?
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Hoarseness, loss of voice
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What is croup?
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Laryngotracheobronchitis
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What are symptoms of croup?
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Hoarseness, barking croup, and stridor
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What is stridor?
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High pitched sound resulting from turbulent air flow in the upper airway
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Where does bronchitis occur in adults?
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In the middle airways
|
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Where does broncitis occur in children?
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In the distal airways (more dangerous)
|
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What are symptoms of bronchiolitis?
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Cough, dyspnea, wheezing
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Where does pneumonia occur?
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Infection of the most distal components of the respiratory tract
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What are some symptoms of pneumonia?
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Cough, chest pain, Rales
|
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Why do viruses preferentially infect certain areas?
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-Specific receptors
-Different temperatures allow for optimal viral growth |
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What percentage of acute respiratory infections does the common cold account for?
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1/3 - 1/2
|
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What are the two most common viruses that cause the common cold?
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Rhinovirus and coronavirus
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What are some other viruses that cause the common cold?
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Adenoviruses, enteroviruses, RSV, influenza, and parainfluenza viruses
|
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How are viruses associated with the common cold transmitted?
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Droplet or direct contact (indirect via objects)
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What is a factor that one can be sure is a predisposition to getting a cold?
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High levels of psychological stress
|
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How do rhinvoviruses often enter the cell?
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Through binding to surface receptor ICAM-1
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Can rhinoviruses kill the cell?
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Not in most cases
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How are antibodies able to exert an effect against the virus?
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They are able to coat the virus, but they are not able to prevent the virus from BINDING to the target cell
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Which viruses typically result in a destruction of the epithelium of the upper airways?
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Adenovirus and influenza
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How long does it take for the damaged epithelium caused by influenza or adenovirus to return to normal?
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7-8 days
|
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What have cold vaccinations typically used?
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Inactivated viral coats
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Why have cold vaccinations typically been found to be inaffective?
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There are 100's of variations against rhinovirus. Also, since the vaccination does not have the normal viral replication machinery, the antibodies produced are not the same as in a viral infection
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What do Rubintrivar and Pleconaril do?
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Drugs that insert into the virus and block their replication
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Where is there alot of bacteria that could have implications in the respiratory system?
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Nasal cavity, saliva, tooth surface and gingival scrapings
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What do the bacteria in these areas comprise?
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They are part of the normal flora (not harmful)
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What is pertussis?
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Whooping cough
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How are people vaccinated to protect against Pertussis?
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-A primary 2-4 months after birth
-A booster at 16-18 months |
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Is immunity against pertussis life-long?
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It is thought that the immunity against pertussis wanes over time
|
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What can these adults with the slightly decreased immunity against pertussis act as?
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Carriers or reservoirs of infection and they can pass along the disease to non-vaccinated or partially vaccinated infants
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In addition to coughing caused by infection of the respiratory tract, what other areas can pertussis affect?
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-Rhinorrhea (runny nose)
-Paroxysmal cough (uncontrolled spasms of coughing) -Lymphocytosis (increased lymphocytes in the blood) |
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What are some less frequent effects of pertussis?
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-Encephalopathy
-Bronchopneumonia |
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How does clinical progression of pertussis begin?
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Runny nose, increased intensity of coughing
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What is the bacteria that causes whooping cough?
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Bordetella pertussis
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Wha tare the two active compounds produced by Bordetella pertussis?
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-Pertussis toxin
-Filamentous hemagglutinin |
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What is important about filamentous hemagglutin produced by the Bordetella pertussis?
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-Colonization of lower respiratory tract
-Immunomodulation |
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What does pertussis toxin do?
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It blocks chemokine receptors and thus inhibits the chemotaxis of neutrophils
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What does this inhibition of chemotaxis by neutrophils result in?
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Delays clearance of bacteria
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How does pertussis toxin kill cells?
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Covalently modifiying essential protein in the host
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What is this covalent modificaiton that occurs as a result of Pertussis toxin?
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Pertussis toxin catalyzes the ADP-ribosylation of alpha subunit of G proteins, leading to IMPAIRED PROTEIN SYNTHESIS
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What is the structural components of Pertussis toxin that are similar to the structures common to potent toxins?
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-B sheets fold on top of each other
-Critical T-2 turn -One side is hydrophobic and the other is hydrophillic |
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Besides inhibiting neutrophil function, how else does pertussis toxin promote their further infiltration into the respiratory tract?
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The pertussis toxin is able to stop the mucocilliary movement of the epithelial lining of the airways, causing disarmament of the mucociliary transport system
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Besides the production of toxins, how else can Pertussis result in impaired mucocilliary transport?
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Endotoxins produced can stimulate non-ciliated cells to produce nitric oxide, which kills the cilliated cells
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What is another term for diptheria?
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Necrotizing tracheobronchitis
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What does diptheria cause?
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Pharyngitis, fever, lymphadenitis, hypoxia, cutaneous diptheria
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How does hypoxia result during diptheria?
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Pseudomembrane obstruction in the upper airways
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What is cutaneous diptheria?
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Infection of the skin
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What are systemic complications of diphtheria?
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-Toxic peripheral neuropathy
-Toxic myocarditis |
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What is toxic peripheral neuropathy?
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Loss of myelin sheaths in the peripheral nerves
|
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What is toxic myocarditis?
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Congestive heart failure
|
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What family does the diphtheria toxin belong to?
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ADP-Ribosyltransferase toxin
|
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What happens when the diphteria toxin is activated?
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The enzymatic domain is released into the cytosol where it interferes with elongation factors
|
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What does this interference with EF's result in?
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The cell is unable to make more proteins, leading to CELL DEATH
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How potent is this diphtheria toxin?
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Only one molecule of this toxin is needed to block the protein synthesis that will result in cell death
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What is a side consequence of this death of cells induced by diptheria toxin?
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The dead epithelial shells will be shed into the airway, and this can cause death by hypoxia
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What are some symptoms of pneumonia?
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Coughing, bloody sputum, chest pain, fever
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What is characteristic of the airspaces in the distal portions of the respiratory tract during pneumonia?
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THey are filled with a mixture of serum and inflammatory cells with the bacteria
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What is pneumonia caused by?
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Bacterial infection
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What is ARDS?
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Adult Respiratory Distress Syndrome
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What is characteristic of ARDS (Adult respiratory distress syndrome)?
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The individual drowns with the inability to breath caused by collection of serum in the alveoli
|
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What does virus binding to ACE cause?
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ACE can no longer protect the lung
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How does ACE protect the lung?
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Converts angiotensin II to AT1-7
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How does the conversion of angiotensin II to AT1-7 result in protection of the lung?
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Angiotensin II binds to AT1aR, which can cause damage to the lung tissue that results in lung edema
|
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Who is most susceptible to pneumonia?
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Infants and young children, and the elderly
-Also those who are fighting a major illness or who are immunosuppresed |
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What are the two main types of pneumonia?
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-Lobar pneumonia
-Bronchial pneumonia |
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What is LOBAR pneumonia typically caused by?
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Infection by Streptococcus pneumoniae
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How does the fibrous exudate in LOBAR pneumonia result?
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In the exudate, fibrinogen is released into the alveoli. This results in the polymerization of fibrin (fibrous)
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How are the fibrin strands eventually removed?
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There is an influx of polymorphs and macrophages that lyse and remove the fibrin strands
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How does the pneumococci bacteria prevent phagocytosis?
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They have a protective CAPSULE
|
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Since these bacteria are able to prevent phagocytosis by their protective capsule, how are they removed?
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A larger amount of Abs must be produced against them in order to allow opsonization and engulphment by macrophages
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What is the difference between lobar and bronchial pneumonia?
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Lobar pneumonia involves the entire lobe of the lung, while bronchial pneumonia involves patches of the lung
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How large of the population is affected by TB?
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1/3 of the population carries a latent form of TB
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Which virus does TB form a lethal combination with?
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HIV - they speed up each others progress
|
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How is tuberculosis transmitted?
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Airborne route
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Who does TB affect the most?
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Young adults in their productive years
|
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Where do most deaths from TB occur?
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50% in Asia
|
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What percentage of people infected with TB have active TB?
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10%
|
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Besides the lungs, what organs can TB infect?
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Lymph nodes, lungs, kidneys, the spine, and the intestine
|
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What is an effective drug against TB?
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Streptomycin
|
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What is the resurgence of TB likely due to?
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Acquired resistance to any of the 4 anti-tuberculosis drugs
|
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What is characteristic of chronic infection of TB?
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Immunity development, granuloma formation, and calcification
|
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How does the TB strain develop drug resistance?
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Chromosomal mutation in the genes responsible for drug resistance
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What is the appropriate therapy against TB?
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Use all four drugs at the same time to avoid resistance
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Where is the site of primary tuberculosis infection?
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Lung or LN's
|
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What can primary infection of tuberculosis cause?
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Pulmonary cavitation (cavities in the upper lobes of the lung)
|
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How does the tuberculosis bacteria cause macrophage inactivation?
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They secrete protein kinase (PknG)
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What does PknG do to inhibit macrophage function?
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It interferes with phagosome fusion to lysosome
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How is tuberculosis testing done?
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Looking for subcutaneous hypersensitivity
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What is COPD?
|
Chronic obstructive pulmonary disease
|
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What is COPD generally caused by?
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It is typically self-induced
|
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What is the most of COPD induced by?
|
Smoking cigarettes (90%)
|
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What are general symptoms of COPD?
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-Inflammation
-Mucus production -Spasm |
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What do these symptoms lead to?
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There is narrowing and disfiguring of the airwyays, and the air is entrapped
|
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What are the three groups of COPD?
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Chronic bronchitis, emphysema, asthma
|
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Which COPD group is generally reversible?
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Asthma
|
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Which COPD group is generally irreversible?
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Emphysema
|
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Why is emphysema generally irreversible?
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THere is destruction of a good portion of the lung tissue and no way to repair it
|
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What is the progression like of airflow limitation?
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Usually progresses with age
|
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How is the reversibility of COPD overall?
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Only partly
|
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What are the basic changes in the airway in COPD?
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Narrowing, plugging by mucus
|
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Why is there increased mucus in COPD?
|
There is hyper secretion of mucus that is secondary to irritation
|
|
Transfer by mortgagor (homeowner) where grantee takes subject to mortgage: assumption
|
Grantee primarily liable and original mortgagor secondarily liable as surety.
|
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What are the initial changes in COPD?
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-Mucus accumulating in the bronchi, loss of recoil, decrease in FEV1
|
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What does the loss of recoil lead to in patients with COPD?
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Cough
|
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What is FEV1?
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Forced expiratory volume in 1 second (the maximal amount of air that can be forcibly blown out)
|
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What are the two main outcomes of COPD on the lungs?
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-Change in lung volume (correlates with decreased FEV1)
-Obstruction leading to trapping of air |
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How is FEV1 used to determine prognosis of COPD?
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The lower FEV1, the more severe the disorder
|
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What is FEV1 indicative of?
|
Post bronchodilator function
|
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What is asthma characterized by?
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Reactive airways
|
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What is the reactive airways in asthma due to?
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Hypersenstive reactions to obnoxious stimuli/irritants in the air
|
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What is occuring in the airways following this hypersenstive reaction?
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There is contraction of the smooth muscle, narrowing the airway, which leads to difficulty in breathing
|
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What are some symptoms of asthma?
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Wheezing, coughing, shortness of breath, sensation of tightness in the chest
|
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What is the highest group of people with asthma?
|
Newborn to age 20
|
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What is characteristic about the smooth muscle spasm in asthma?
|
There is a smooth muscle spasm, leading to further constriction
|
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What happens to the mucus in asthma?
|
Mucus levels increase, and dry out when breathing, forming a plug
|
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What are some etiological agents that can trigger an asthma attack?
|
Bugs, pollutants, pollen, smoking, respiratory tract infection, emotional distress, exercise, food additives, animal dander, mold, certain medicines, extreme weather/cold air
|
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Why does emotional distress lead to asthma attacks?
|
There is a high CNS control of innervation to the lung
|
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What type of effect does cold air have on an asthmatic lung?
|
It sends it into "spasm"
|
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How can one treat asthma?
|
Use bronchodilators
|
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What happens if the narrowed airway with edema, mucus and inflammation, contracted smooth muscle?
|
-Hyperplasia of the smooth muscle
-Fibrosis |
|
What is "remodelling of airways"?
|
Typically occurs in adults with chronic asthma and involves an increase in muscle around the wall of the airway
|
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What is the first drop in FEV during asthma caused by?
|
Release of mediators such as histamine
|
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What is the later dropping in FEV-1 associated with?
|
The presence of inflammatory cells:
TH2 cells releasing cytokines Eosinophils Neutrophils |
|
What is the first drop in FEV-1 responsive to?
|
Nor-adrenaline
|
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What is the second drop responsive to?
|
Cortico-steroids
|
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What is one of the crucial points of pathophysiology?
|
Hyperresponsiveness of airway muscle
|
|
What are some agonists that cause smooth cell contraction in asthma?
|
Histamine, acetylcholine
|
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How can someone with asthma develop a reaction quickly?
|
When being exposed to a noxious stimulus
|
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When is a person with asthma particularly sensitive to bronchospasms?
|
After a cold, the person gets into an asthmatic state
|
|
What are the components of the acute inflammatory response in asthma?
|
Broncho-constriction, edema, secretions, cough
|
|
What are the components to the chronic inflammatory phase in asthma?
|
There is cell recruitment, epithelial damage, and early structural changes in the lung
|
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What is the epithelial cell damage caused by in the chronic inflammatory phase in asthma?
|
Eosinophils
|
|
What are some of the components of the airway remodeling?
|
Cellular proliferation, extracellular matrix increase, increase in fibrous tissue, increase in smooth uscle
|
|
What does the presence of neutrophils in the airway cause?
|
Mucus secretion
|
|
What does the presence of eosinophils in the airway result in?
|
The eosinophils degranulate causing ulceration to the lung
|
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What is "status asthmaticus"?
|
A SEVERE asthma attack in which there is no way to break spasm (ie. cannot use bronchodilators or steroids to fix it)
|
|
How must status asthmaticus be treated?
|
Lungs must be washed out to clean mucus
|
|
When does asthma become irreversible?
|
When the airway remodeling occurs in someone that has been asthmatic for a long time
|
|
What does eosinophil induced necrosis of epithelal cells do?
|
This activates myofibroblasts which can either form MUSCLE of FIBROUS CELLS
|
|
Which T cell seems to be more important in asthma?
|
Th17
|
|
What is corticosteroids inhaled with?
|
Beta 2-agonist (bronchodilator)
|
|
How does smoking increase COPD and cancer?
|
Induces inflammation in the lungs
|
|
What are the changes in the airway common to chronic bronchitis and emphysema?
|
Hyper secretions of mucus
Smooth muscle increase in walls of airways, leading to spasm and constriction |
|
How does PCO2 increase in patients with chronic bronchitis?
|
The airflow is blocked, and the air is stuck in the lungs. Thus the PCO2 in the blood goes up
|
|
Why is there increase mucus production in patients with chronic bronchitis and emphysema (induced by smoking)?
|
The goblet cells become the majority, resulting in a massive production of mucus
|
|
What happens to the squamous epithelium due to smoking?
|
It undergoes squamous metaplasia due to irritation from smoking
|
|
What is the difference between chronic asthma, bronchitis with emphysema?
|
In emphysema there is no airway modeling or modification, there is simply airway DESTRUCTION
|
|
Why does air become trapped in the alveoli and alveolar ducts in emphysema?
|
The normal recoil is missing since there is no elastic tissue remaining
|
|
What are symptoms of emphysema?
|
Limited physical exertion
Difficulty exhaling Shortness of breath |
|
What are some changes in lung function?
|
Total lung capacity
Tital volume Functional residual capacity |
|
What causes these changes in lung function in emphysema?
|
Dilation and destruction of distal air ways and entrapment of air
|
|
What happens to the extra respiratory muscle as a result of difficulty breathing?
|
Extra respiratory muscles are hypertrophied, and the person becomes "barrel chested"
|
|
Which component of lung function is "ok" in emphysema?
|
Tidal breathing (volume of air that is inhaled and exhaled in normal, resting breath)
|
|
What are the two divisions of emphysema?
|
Centrilobular
Panlobular |
|
What type of lesion is centrilobular emphysema?
|
Lesion in the centre
|
|
What is panlobular emphysema?
|
Involves the whole lobe
|
|
How can a pneumothorax result during emphysema?
|
A bubble forms, and it breaks resulting in air in the pleural space and lung collapse
|
|
Why is a patient with emphysema more likely to die from pneumothorax than someone without?
|
The reserve is so low that the other lung cannot accomodate and the person dies rapidly
|
|
How much of the gas exchange area is lost in emphysema?
|
80%
|
|
What happens when the elastic tissue is lost in a patient with emphysema?
|
-There is lower alveolar pressure
-THere is reduced radial traction |
|
What does the lower alveolar pressure and reduced radial traction lead to?
|
Collapsed airway and difficulty breathing out
|
|
What is a consequence of the individual being unable to breath out?
|
Air becomes trapped in the lungs, leading to lack of normal gas exchange, and the development of hypoxia
|
|
What is the pathogenesis of emphysema thought to be caused by?
|
The release of elastases by neutrophils that is caused by the inflammation induced by tobacco
|
|
How does smoking induce upregulation of ceramide in the epithelium?
|
Smoking induces oxidative stress and the release of H2O2, which causes activation of neural sphingomyelinase, which causes the release of ceramide from sphingomyelin.
|
|
What does the upregulation of ceramide induce?
|
Increased apoptosis of cells, leading to damage of airways
|
|
What is hereditary emphysema?
|
Caused by a hereditary loss of alpha-1 antitrypsin anti-proteases
|
|
What is characteristic of restrictive lung disease?
|
The lung becomes fibrotic due to a number of different agents and the person unable to inhale or exhale because the lung is a mass of fibrous tissue
|
|
What are some symptoms of restrictive lung disease?
|
Clubbing in fingers
Hypoxic cyanotic Unable to breath |
|
What is restrictive lung disease typically a result of?
|
CHronic airway disease (not smoking)
|
|
What is the lung compliance like in an individual with fibrosis?
|
They have little lung compliance
|
|
How does activation of the immune system result in the development of fibrous tissue?
|
Chemotactic cytokines can act on fibroblasts, causing an increase in fibrous tissue formation
|
|
How does pseudonomas aeruginosa infection in cystic fibrosis patients prevent neutrophil function?
|
The neutrophils are killed by the bacteria, and they release proteases, which cleave CXCR1 which disarm the neutrophils
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What is LPA?
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Lysophosphatidic acid
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What does increase levels of LPA result in?
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Increased vascular leakage and fibroblast recruitment
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Why is the lung of a person with restricted lung disease referred to as a honey comb lung?
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There is a lot of fibrous tissue, with large spaces and inflammatory reactions
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