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Health Studies > Asthma Roop/Raja > Flashcards

Asthma Roop/Raja Flashcards

1
Q

What is wheezing?

A

Whistling sound upon expiration because of an obstruction

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2
Q

What are the primary causes of wheezing?

A

-Asthma
-Bronchitis
-COPD

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3
Q

What might a physical exam show for a pt wheezing, anxious, and SOB?

A

-wheezing is more prominent on exhalation and there is an extended forced expiratory phase
-chest anteroposterior diameter appears large for age and size
-nasal mucosa is edematous, and the pharynx is coated w/ a clear postnasal discharge

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4
Q

A pt who is wheezing may be prescribed a beta-2-adrenergic agent administered by an inhaler, and the symptoms quickly subside. Beta 2 agonists replicate the actions of the catecholamines. Name the catecholamines and what are the actions of beta 2 agonists?

A

Catecholamines = NE and Epi

action= dilation by relaxing smooth muscle on multiple organs

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5
Q

What causes the large diameter of the anteroposterior chest for some patients wheezing?

A

-Air trapped in lungs → increases lung size → pushes chest out
-When you inspire→ chest wall pushes out (issue is that we can’t get the air out bc muscles are contracting)

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6
Q

What are the 3 types of beta receptors?

A

beta 1, 2, and 3

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7
Q

Do beta 1 receptors increase or decrease cAMP? What organs are affected and how?

A

beta 1 receptors increase cAMP

affects heart (increase co) and kidneys (increase renin)

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8
Q

Do beta 2 receptors increase or decrease cAMP? What organs are affected and how?

A

beta 2 receptors increase cAMP

smooth muscle relaxation–> lungs, blood vessels, GI tract, bladder, uterus, liver

will increase diameter of lungs and blood vessels

will decrease peristalsis and digestion

bladder will decrease urination

liver will make glucose

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9
Q

Do beta 3 receptors increase or decrease cAMP? What organs are affected and how?

A

beta 3 receptors increase cAMP

affects adipose tissue and bladder

there will be lipolysis and decreased urination

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10
Q

What does Gs mean?

A

increases cAMP

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11
Q

Beta1= heart= _________
Beta2= lungs= ________

A

1 heart, 2 lungs

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12
Q

What are the pulmonary function tests?

A

-spirometry test
-methacholine challenge test (bronchoprovocation test)

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13
Q

What is spirometry?

A

-Measurement of lung capacity
-Expiring into tube and spirogram measures
-Only exhalation
-Measuring how much air you can breathe out in one forced breath

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14
Q

What is a methacholine challenge test and what is methacholine?

A

-Methacholine is a parasympathomimetic bronchoconstrictor used to diagnose bronchial hyperreactivity in subjects who do not have clinically apparent asthma

-during the test, pt will be asked to inhale doses of methacholine, a drug that can cause narrowing of the airways. A breathing test will be repeated after each dose of methacholine to measure the degree of narrowing or constriction of the airways

-Methacholine is administered sequentially in increasing conc.

-Methacholine is also known as Acetyl-β-methylcholine, which is a synthetic choline ester that acts as a non-selective muscarinic receptor agonist in the parasympathetic nervous system (airways are obstructed and they try to get air out)

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15
Q

What can you expect during a spirometry test?

A
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16
Q

A pt undergoes a methacholine test. The results show hyperreactive bronchoconstriction with decreased FEV1, decreased forced vital capacity and increased residual volume. Flow/volume loop demonstrates scooping. What is FEV1 and what is scooping?

A

forced expiratory volume (1 = first second)

FEV1 = vol. of air that can be expired in the first second of a forced maximal expiration

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17
Q

Is asthma obstructive or restrictive?

A

obstructive (fibrotic lung disease would be restrictive)

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18
Q

What is forced vital capacity (FVC)?

A

volume of air that can be forcibly expired after a maximal inspiration = TV +IRV+ERV

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19
Q

FEV1 is normally _____% of forced vital capacity. What is the equation here?

A

80%

FEV1/FVC = 0.8

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20
Q

In _____________ lung disease, FEV1 is reduced so FEV1/FVC is decreased

A

obstructive

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21
Q

Asthma is a chronic inflammatory disease of the airways that includes….

A
  • Airway hyperresponsiveness (airway narrowing) to specific triggers
  • Chest tightness
  • Variable airflow limitation
  • Coughing
  • Wheezing
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22
Q

What are some asthmatic triggers?

A

-Pollen
-Dust
-Pet hair
-Grass
-Shellfish and nuts- breathing it in, not eating
-Smoking/ second hand smoke

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23
Q

What type of epithelium lines the majority of the airways?

A

Pseudostratified ciliated columnar epithelium with goblet cells = RESPIRATORY epithelium

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24
Q

Goblet cells produce mucus for what purpose?

A

to trap pathogens/allergens

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25
Q

What is the function of the cilia in respiratory epithelium?

A

moving mucus up to the mouth to expectorate (spit it out) or swallowing through a mucociliary escalator

note: mucociliary escalator stops working in asthma bc of constant inflammation

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26
Q

Do respiratory alveoli and bronchi have cilia? explain

A

no

instead of cilia, there are macrophages to help remove mucus→ dust cells (which are the macrophages of the lungs)

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27
Q

What type of epithelium is lining the respiratory alveoli and bronchi?

A

simple squamous epithelium

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28
Q

What keeps the respiratory cells together but are disrupted in pts with asthma (pathogens can get through)?

A

Tight junctions and adherens junctions

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29
Q

On each side of respiratory epithelium there are cells from innate and adaptive immunity. What cells are they specifically?

A

-Innate = dendrites, granulocytes, macrophages, mast cells, NK cells
-Adaptive = B/T cells (CD4 = helper T cell)

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30
Q

When asthmatics are exposed to allergens, the allergens will pass by the cells/breach them because the tight junctions and adherens junctions are lost. Nothing will move the allergens out of the way, and so it sets up a reaction for who? What does this trigger?

A

SENSITIZED individuals

eosinophils and interleukins will be released as a result of this

which will result in an increase in fibrosis and cause a thickening under the basement membrane of airways

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31
Q

The epithelial-derived cytokines TSLP, IL-33, and IL-25 are released in response to allergens and respiratory viruses and act as key upstream drivers of _________ inflammation in the airways through effects on both innate and adaptive immune cells.

A

type 2

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32
Q

How is respiratory epithelium disrupted in asthmatics?
hint: 3 things

A

1) disruption of tight junctions
2) detachment of ciliated cells
3) reduced expression of cell to cell adhesion molecules such as E-cadherin

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33
Q

What is the pathophysiology of asthma?
hint: 3 things

A

1) airway inflammation
2) intermittent airflow obstruction
3) bronchial hyperresponsiveness

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34
Q

What happens in airway inflammation?

A

-production of increased airway responsiveness
-produce airway edema and cause the immigration of inflammatory cells into the lumen through the epithelium
-Mast cells and basophils release histamine (histamine is one of the primary mediators)
-Prostaglandins + histamine → causes obstruction

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35
Q

What are the 4 things seen with airway inflammation?

A

1) edema and mucus secretion (both leading to obstruction)
2) desquamation of the epithelium
3) smooth muscle hyperplasia (smooth muscle shouldn’t be thick (hyperplasia) in terminal bronchioles)
4) eosinophil infiltration

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36
Q

What happens in airway obstruction (specifically asthma)?

A

-happens when you can’t move air in or out of your lungs
-caused by smooth muscle hyperplasia (smooth muscle shouldn’t be thick in terminal bronchioles)
-bronchoconstriction will affect the airways

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37
Q

What antibody is produced during airway obstruction (bronchospasm)? What does it do?

A

IgE

IgE production triggers the release of inflammatory mediators like histamine and leukotrienes

These result in bronchospasm (smooth muscle contraction in the airways) and edema

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38
Q

What is bronchial hyperresponsiveness?

A

Excessive narrowing of airways resulting in increased airway resistance and decreased airflow

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39
Q

What is Poiseuille’s Law?

A

-Note the inverse fourth power relationship between resistance and the radius of the airway. Therefore if airway radius decreases by a factor of
4, then resistance will increased by a factor of 256, and airflow will decrease by a factor of 256.
-Resistance affected by the radius (to the fourth power)
-L= length of the airway
r = radius of the airway
n = viscosity of the inspired gas

40
Q

What signs and symptoms indicates increased resistance in asthmatic patients?

A

Wheezing and SOB

41
Q

T/F:

At rest, you should have equal pressure outside and inside of lungs

A

true!

42
Q

With inspiration, diaphragm moves down and volume increases. What happens to pressure?

A

it decreases (air flows in)

43
Q

During expiration (remember that it is a passive movement), diaphragm moves up and volume decreases. What happens to pressure?

A

it increases (higher than atm pressure, so air will move out)

44
Q

Is inspiration normal in asthmatic pts?

A

yes (expiration is what they struggle with)

45
Q

What is wrong with the airway for asthmatic pts?

A

there’s an airway obstruction

46
Q

Asthmatic patients will have increased resistance on airways due to increased pressure. What can happen as a result?

A

if pressure increases too much, then the airways will collapse

or

air becomes trapped in alveoli (narrowed lumen and increase in smooth muscle)

air that should be expired is not, resulting in air trapping and increased FRC (w/ FEV1/FVC)

47
Q

What symptoms does an asthmatic have when there is air trapping in alveoli/lungs?

A

-Increased diameter
-Tightness in chest → because of air trapped in alveoli

48
Q

What happens to the airway smooth muscle w/ severe asthma?

A

-hyperresponsiveness
-constriction
-thickening

49
Q

What are the characteristics of severe asthma compared to healthy airway?

A
50
Q

What is the typical tx for asthma?

A

Beta 2 agonist → relaxed airways, HR and respiration decreases

51
Q

Asthma can be managed and monitored, but can asthma still be fatal in the western world today?

A

YES

52
Q

What is the deadly triad of asthma?

A

1) respiratory exhaustion (airways are not opening with dilator and air is trapped inside)
2) respiratory acidosis (CO2 build up)
3) impaired venous return (decreased venous return in asthmatics)

53
Q

Asthma is what type of allergic disease?

A

IgE mediated allergic disease

54
Q

Do allergies always have some type of immunological response?

A

yes

55
Q

Abundance of IgE production/presence of IgE leads to some immunological response in what type of diseases?

A

IgE-mediated allergic diseases

56
Q

Asthma complicates IgE-mediated allergic diseases. How/why?

A

-Massive immune response that the body has towards the allergen
-Mediated by the antibodies

57
Q

Genetic aberrations in certain entities can put someone at risk for an ___________ reaction. Environmental factors can also be a cause. Combination of what we’re exposed to over time + genetics = contributes to how we respond to the foreign entity/allergen that we’ll encounter

A

asthmatic

58
Q

The route of entry is important for asthmatic patients when they come in contact with an allergen (inhalation leading to contact w/ mucosal lining of lower airways). This will lead to…..

A

-bronchoconstriction
-increased mucus production
-airway inflammation
-bronchial hyperreactivity.

59
Q

________________ involves class switching to IgE production on first contact with an allergen

A

Sensitization

60
Q

Genetic factors contribute to the development of __________________ disease.

A

IgE-mediated allergic

61
Q

Environmental factors may interact with ___________ susceptibility to cause allergic disease.

A

genetic

62
Q

What are the 3 asthma susceptibility loci?

A

1) genes expressed in airway epithelial cells (affects chemokines, and antimicrobial peptide production)
2) genes regulating CD4 T cells and ILC2 differentiation and function (affects cytokine production and pattern recognition receptors (PRRs))
3) genes w/ other functions (affects other signaling protein release)

63
Q

What does atopic generally mean?

A

exaggerated immune response

64
Q

Atopic conditions most often involve which antibody?

A

IgE

65
Q

Environment: “the more you expose your body to different environments, less susceptible to atopic reactions”. This is referring to hygienic vs non-hygienic. Explain this

A

Hygienic → more susceptible for atopic

“Less hygienic” → will not respond in an exaggerated fashion

More exposure → body learns to fine tune how to respond to the allergen

66
Q

What are the features/characteristics of airborne allergens that may promote the priming of TH2 cells that drive IgE responses?

A

-proteins, often with carb side chains (protein antigens induce T cell responses)
-low dose (favors activation of IL4-producing CD4 T cells
-low molecular mass (allergen can diffuse out of particles into the mucosa)
-highly soluble (allergen can be readily eluted from particle)
-stable (allergen can survive in desiccated particle)
-contains peptides that bind host MHC class II (required for T-cell priming)

67
Q

The 2 key cells that get activated in IgE mediated allergic diseases are….

A

T follicular helper cells and TH2 cells

68
Q

TFH cells promote production of antibodies. How?

A

-Specialized subset of CD4 T cells that release IL-21 to the B cell to help them generate antibodies
-Has to produce IL21 (brings B cells to area)
-Activates B cells
»Differentiate and proliferate to produce antibodies (IgE for asthma)
»To produce IgE → has to produce a specific interleukin first! (IL21)

69
Q

TH2 cell activation leads to cytokine release to do what?

A

-Th2 cells express a range of cytokines that influence B cell differentiation and antibody production
-Activated by APCs
-Dendritic cells (sentinel cells) sees something foreign first
»Receptor on the dendritic cell saw the pollen
»Processes it and shows it to t helper cell
-Dendritic cells release IL4 to recruit Th2 cells because of the extracellular antigen
-macrophages produces IL 4, IL 5 → calling eosinophils, basophils and mast cells
»Also tells goblet cells to produce mucus = xs mucus

70
Q

The first exposure to pollen will allow IL4 to drive B cells to produce IgE in response to pollen antigens. What happens next?

A

-pollen-specific IgE binds to mast cells
-second exposure to pollen will then result in an acute release of mast cell contents that cause allergic rhinitis (hay fever)

71
Q

The enzyme Der p 1 cleaves occludin in tight junctions and enters mucosa. Der p 1 is taken up by dendritic cells for antigen presentation and T-cell priming. What happens next?

A
72
Q

Mast cells reside in tissues and orchestrate allergic reactions w/ release of histamine. How? What happens following the release?

A

-IgE has to bind to Fc receptor on mast cell
-Free floating antibody will only bind to Fc on mast cell with an antigen attached (pollen)
»Lyn Syk pathway
»Tyrosine kinase → autophosphorylation
»LAT activates PLC (phospholipase C) → activates PIP3, switch over to PIP2 → IP3 → attaches to protein on ER → opens calcium channels → xs calcium ions force the granules to fuse with membrane and release
»»Cholera toxin impacts this pathway
-Signal transduction
-Tells mast cells to release granules (contains histamine and other entities)
»Histamine bronchoconstricts
»Also release a series of cytokines:
»»IL 4 = keep activating TH4- cyclical and promote each other
»»CCL3 → calls more macrophages and neutrophils
»»Prostaglandins → vasodilator
»»Leukotrienes → recruit WBC

73
Q

Crosslinking of Fc epsilon RI by allergen recruits and activates the Syk tyrosine kinase. What happens next?

A

-Syk phosphorylates LAT, which recruits and activates PLC gamma
-Activated PLC gamma generates IP3 which causes calcium release from the ER stores
-cytosolic calcium induces secretion of the contents of the mast cells performed granules

74
Q

Mast cell activation and granule release will enter the eyes, nasal passages, and airways. What happens to the eyes, nasal passages, and airways?

A
75
Q

Histamine is a toxic mediator. What are its biological effects?

A

-toxic to parasites
-increases vascular permeability
-causes smooth muscle contraction
-anticoagulation

76
Q

IL4 is a cytokine that will have what biological effects?

A

stimulate and amplify TH2 cell response

77
Q

Prostaglandins and leukotrienes are lipid mediators that will have what biological effects?

A

-smooth muscle contraction
-chemotaxis of eosinophils, basophils, and TH2 cells
-increase vascular permeability
-stimulate mucus secretion
-bronchoconstriction

78
Q

Eosinophils and basophils cause inflammation and tissue damage in allergic reactions. How?

A

-Kicked up when macrophages cannot engulf
»Usually eosinophils = parasites
-Similar pathway to mast cells
-Presence of IgE → cross link with pollen → binds to Fc on eosinophils
-What is released?
»IL4
»CXCl8 → pulls more leukocytes in (extravasation)
»Major basic protein → triggers histamine release from mast cells

79
Q

Describe an acute response for allergic reactions

A

-inflammatory mediators cause increased mucus secretion and smooth muscle contraction leading to airway obstruction
-recruitment of cells from the circulation

80
Q

Describe a chronic response for allergic reactions

A

chronic response is caused by cytokines and eosinophil products

81
Q

What are the biological effects of major basic protein?

A

-toxic to parasites and mammalian cells
-triggers histamine release from mast cells

82
Q

What are the biological effects of cytokines such as IL4, IL13, IL3, and GM CSF?

A

-amplify eosinophil production by bone marrow
-eosinophil activation

83
Q

What are the biological effects of chemokines such as CXCL8 (IL8)?

A

promotes influx of leukocytes

84
Q

What are the biological effects of lipid mediators such as leukotrienes C4, D4, and E4?

A

-smooth muscle contraction
-increase vascular permeability
-increase mucus secretion
-bronchoconstriction

85
Q

Allergen inhalation is associated with the development of _________ and __________

A

rhinitis, asthma

86
Q

Allergen introduced into the bloodstream can cause ____________ and ___________

A

anaphylaxis, urticaria

87
Q

IgE-mediated allergic reactions have a _______ onset but can also lead to ________ responses.

A

rapid, chronic

88
Q

What is the difference between allergic rhinitis and asthma?

A

allergic rhinitis (upper airway) is caused by increased mucus production and nasal irritation

asthma (lower airway) is due to contraction of bronchial smooth muscle and increased mucus secretion

89
Q

IgE mediated allergic disease can be treated by inhibiting effector pathways, such as with….?

A

-Inhalers
-biologics
-leukotriene modifiers
-corticosteroids
-allergy meds (Claritin D or Zyrtec)
-immunotherapies

90
Q

What is Claritin D MOA? How is it used to treat asthma?

A

-blocks the action of histamine
-contains a decongestant and is also used to treat nasal congestion and sinus pressure

91
Q

What are biologics and how do they work?

A

-massive class of drugs that are all antibody therapeutics
-giving antibodies against IgE (anti IgE)
-clump up IgE → will not bind to antigen (will not bind to mast cell/basophil)
-EXPENSIVE!
-Omalizumab (asthma biologic)

92
Q

What do leukotriene modifiers do?

A

ensuring leukotrienes aren’t being produced

93
Q

What do corticosteroids do when being used for asthma/allergic reactions?

A

ensure prostaglandins and leukotrienes aren’t released, to reduce inflammation

94
Q

When are immunotherapies used?

A

for low dosage infections

95
Q

What are the 4 clinical uses of treatments for allergic disease?

A
96
Q

What disintegrates with asthma?

A

antimicrobial peptides (AMPs)

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