BMS 250 test 2 Flashcards
What is allergic rhinitis
An allergy is a heightened sensitivity to an allergen (foreign protein)
Rhinitis is an eosinophilic inflammation from IgE-mediated reaction
Allergic rhinitis is both
the onset of allergic rhinitis necessitates an initial phase of _____?
sensitization
Allergic rhinitis is what type of hypersensitivity reaction?
Type 1
Type I hypersensitivities include atopic diseases, which are an exaggerated IgE mediated immune responses (i.e., allergic: asthma, rhinitis, conjunctivitis, and dermatitis), and allergic diseases, which are immune responses to foreign allergens (i.e., anaphylaxis, urticaria, angioedema, food, and drug allergies).
describe pathophysiology of allergic rhinitis after sensitization occurs?
an APC (like dentritic cell, macrophage, or langerhan cell) presents low dose antigen to helper T lymphocyte.
Activated helper T lymphocyte produces cytokines IL-3, IL-5, IL-13 that engage with B lymphocytes, instigating allergen specific IgE
upon exposure in allergic rhinitis, where does the specific antigen bind? (early phase response)
IgE antibodies on mast cells that were already there. So the previously fixated IgE molecyles identify the allergens and trigger mast cell activation.
What elicits sneezing and congestion
sneezing: mast cell degranulation -> histamine stimulates the sensory nerve endings on the Vth nerve (trigeminal).
congestion: histamine + leukotrines and prostaglandins = dilation of blood vessels and mucus secretion
how long after the early phase response do you see the late phase response?
4-6 hours after antigen stimulation
how long are symptoms prolonged and what mediators contributions to the persistence of symptoms?
18 to 24 hours.
release of cytokines and leukotrienes -> influx of inflammatory cells into affected area (chemotaxis).
Mast cells and cytokines IL-4, 5 and 13 (type 2 response) are needed to orchestrate the late phase response. what do these cytokines upregulate expression of?
expression of adhesion molecules like VCAM-1 on the endothelial cells.
This faciliates infiltration of eosinophils, T-lymphocytes, and basophils in nasal mucosa.
summary of early phase response in allergic rhinitis
- Antigens (e.g., pollen, mites, pet hair) bind to IgE antibodies on mast cells.
- Mast cells release histamine, leukotrienes, tryptase, kinins, and prostaglandins.
- Histamine and leukotrienes bind to their respective receptors on target cells, causing symptoms like inflammation and bronchoconstriction.
- Antihistamines and leukotriene receptor antagonists block these pathways to alleviate symptoms.
summary of late phase response in allergic rhinitis?
- Eosinophils release cationic proteins and cytokines, contributing to tissue damage and chronic inflammation.
- Basophils enhance the response with histamine and other cytokines
What role do commensal bacteria play in a healthy gut microbiome?
They contribute to the production of short-chain fatty acids (SCFAs), which help regulate immunity and maintain gut health.
How does IgA secretion support gut health?
IgA antibodies protect against pathogens by neutralizing harmful bacteria and maintaining gut homeostasis.
Which immune cells are responsible for maintaining immune tolerance in a healthy gut microbiome?
T regulatory (Treg) cells.
What is the function of IL-22 in gut health?
L-22 promotes epithelial health and defense mechanisms.
How does an increase in non-commensal bacteria affect the gut?
It leads to epithelial damage and immune dysregulation.
Disrupted epithelial barrier: Leads to increased permeability and heightened immune activation
Which immune response is activated in a dysregulated gut microbiome that contributes to allergic rhinitis?
Th2 cell activation, driven by IL-4 and IL-13.
What type of antibody is overproduced in allergic rhinitis due to Th2 cell activation?
IgE antibodies.
In AR there is a reduced gut microbiome diversity.
T/F: More abundant Bacteroidetes and reduced Firmicutes
true
Bacteroidetes: Increased levels of this phylum are associated with inflammation and altered gut function.
Firmicutes: Reduced levels are often linked to gut dysbiosis and decreased production of beneficial metabolites like short-chain fatty acids (SCFAs), which are crucial for maintaining gut health and immune regulation.
what is perennial allergic rhinitis
constant, no seaonsal variation
Grade 1 adenoid hypertrophy
Milder presentation with slight swelling of the mucosa.
Minimal obstruction or deformation.
Indicates early-stage inflammation or polyp development.
Grade 2 adenoid hypertrophy
More prominent swelling or multiple larger polyps.
Greater obstruction and structural deformation visible.
Suggests a more advanced stage of the condition
Grade 3 adenoid hypertrophy
Larger, more prominent swelling or polyps.
Significant obstruction visible, with increased redness and vascularity.
Indicates advanced inflammation, causing considerable disruption to normal anatomy.
Grade 4 adenoid hypertrophy
Severe polyp formation or inflammation completely obstructing the view.
Marked redness, smooth or edematous surfaces, and loss of normal mucosal landmarks.
Suggests end-stage disease requiring urgent intervention (e.g., surgery).
most common symptoms of nonallergic rhinitis
nasal obstruction and clear rhinorrhea. less common sneezing itchy water eyes like allergic
what is the most common form of non-allergic rhinnitis seen clinically?
a. occupational
b. viral
c. vasomotor
d. nonallergic rhinitis with eosinophillia
c. vasomotor or idiopathic rhinitis
Vasomotor rhinitis (VMR) is a non-allergic, non-infectious form of chronic rhinitis caused by dysregulation of the autonomic nervous system, leading to abnormal nasal vascular and glandular responses. VMR is triggered by nonspecific environmental factors such as:
Temperature changes
Humidity fluctuations
Strong odors (perfumes, smoke)
Stress
Spicy foods
mucous secretion and vascular tone are governed by what divisions of autonomic NS
mucous - parasympathetic (acetylcholine)
vascular tone - sympathetic (NE and neuropeptide Y)
what is NARES?
nonallergic rhinitis with eosinophillia
High eosinophil levels (above 25%) but no elevated serum IgE distinguishing it from allergic rhinitis. Unknown in cause.
what is rhinitis medicamentosa?
overuse of topical nasal decongestants like oxymetazoline and phenylephrine
aka rebound congestion.
Why can pregnancy cause rhinitis?
estrogen concentrations increase. In nasal tissue estrogen can increase amount of hyaluronic acid. similar symptoms can appear premenstually.
definition of chronic rhinosinusitis
inflammation of nasal cavity and paranasal sinuses lasting more than 12 weeks
clinical features of chronic Rhinosinusitis
purulent discharge - green or yellow
facial pain/dental pain
nasal obstruction
hyposmia (sense of smell)
fever
polyps
what causes the majority of nasal polyps?
Th2 cell driven eosinophilia, IgE, elevated IL-5
functional changes with age
clinical features of nasal polyps
progressive nasal obstruction and facial congestion, hyposmia and rhinorrhea
clinical presentation of nasal septal deviation
headachesm rhinosinutis, high BP, OSA, breathing sounds
most common cause of pharyngotonsillitis?
viral infections (70 to 85%) of acute causes.
adenovirus, rhinovirus, covid, EBVs, HIV, HSV, influenza
what does a spirometry measure?
Lung volumes and airflow
- forced expiratory volume in 1 second FEV1
- Forced vital capacity FVC
- ratio of FEV1/FVC
used for obstructive lung diseases like asthma and COPD
what does a body plethysmography measure?
total lung capacity TLC
residual volume RV
and air way resistance
used for both obstructive and restrictive lung diseases
overall more complete assessment than spirometry
how are obstructive lung diseases clinically defined?
decreased FEV1/FVC ratio
increased RV and FRC
normal total lung capacity
how are restrictive lung diseases clinically defined?
physiological FEV1/FVC ratio
decreased RV and FRC
decreased total lung capacity
what is bronchial asthma ‘Trias’ definition?
chronic inflammation
obstructive ventilatory impairment + bronchial hyper responsiveness
Reversibility of impairment
what drug is a common trigger of bronchoconstriction?
aspirin
new classification of asthma is allergic vs non allergic. What are the 5 types of asthma?
- allergic - atopic
- nonallergic
- drug induced
- occupational
- cardiac
what is the mechanism of allergic asthma?
Type 1 hypersensitivity reaction
hyper reactive airways that constrict in response to stimuli, causing increased airway resistance
pathway of a type 1 hypersenstivity?
CD4 + Th2 cells release IL-4 and IL-5 -> stimulate eosinophils -> production of IgE
what is a common trigger of nonallergic asthma?
viral infection like rhinovirus, parainfluenza virus
what are the T helper cells involved in nonallergic asthma
Th17 and Th1 that recruit neutrophils
what mediators are involved in the early stage of asthma?
mediators that promote bronchoconstriction:
- leukotrienes
- histamine
- prostaglandins
what mediators are involved in the late stage of asthma?
eosinophils that release major basic protein (toxic to epithelial cells)
and neutrophils that release proteases
what is the late stage of asthma responsible for?
the morphologic changes that occur
- hypertrophy of smooth muscle
- increased collagen under BM
- hyperplasia of mucous glands
- eosinophilic infiltrate
describe the pathology of airway obstruction
reduced airway lumen
smooth muscle constriction
mucus
thickening of SUBmucosa: edema and cellular infiltration
what are the 2 components of airway hyperresponsiveness?
- functional - hyperresponsivness of airway smooth muscle reaction to histamine or methacholine
- structural - airway wall thickness
T/F: the lungs becomes hyperinflated in asthma
true, they press against the chest wall and can leave indentations in the lung fro the ribs
what are charcot-leyden crystals and curschmann spirals
charcot-leyden crystals- major basic protein
curschmann spirals - sloughed epithelial cells in mucous cast in shape of airway
what is mucous plugging?
a characteristic feature of status asthmaticus. If the curschmann spirals aren’t able to leave, they will plug up the alveoli, creating a mucus plug.
Reduces the gas exchange surface area.
what are spirometry findings during an asthma exacerbation
reduced FEV1/FVC
reduced PEF peak expiratory flow
increased RV residual volume
what would the spirometry findings be BETWEEN exacerbations in early asthma vs late?
early - findings are normal
late - decreased PEF and FEV1/FVC, increased RV
during a exacerbation will Co2 be high or low?
low because hyperventilation -> increased respiratory rate leads to excessive CO₂ exhalation, causing a low arterial CO₂ (hypocapnia) and respiratory alkalosis.
Due to impaired oxygen exchange, hypoxia stimulates the brainstem to increase ventilation, further lowering CO₂
why is high or low Co2 concerning?
Low CO₂ → Common in mild-to-moderate asthma exacerbation (due to hyperventilation).
Normal or High CO₂ → BAD SIGN! Suggests respiratory fatigue and impending failure.
what is the classic triad of asthma
wheezing
dyspnea
cough (worse at night)
why is the cough worse at night?
because there is a drop in cortisol at night, cortisol usually helps your lungs stay open. when it drops you have the symptoms.
T/F: COPD is preventable but irreversible
true
its characterized by airflow limitation that is not fully reversible. the airflow limitation is usually progressive
what is the gene that is a risk factor for COPD
alpha-1 antitrypsin deficiency
trypsin - a protease, breaks down protein. without the antitrypsin -> increased breaking down of connective tissue and lung tissue gets thinner and thinner
what is the single most important risk factor for COPD?
smoking (active and passive)
what is the key risk factor for COPD?
cumulative exposure to noxious particles
- like smoking, indoor air pollution, occupational dusts, outdoor air pollution. like everything at once.
what is the definition of chronic bronchitis
productive cough for at least 3 months in 2 consecutive years
definition of emphysema
loss of pulmonary parenchyma
- loss of alveolar septae and walls of airways and dilation of terminal airways
what is the mechanims of emphysema?
loss of pulmonary parenchyma
-> loss of elastic recoil
-> exhale: airways collapse
-> air trapping
leads to dilation of airspaces and bullae form
what is centriacinar emphysema
smoking
respiratory bronchioles in the upper lobes
what is panacinar emphysema
alpha-antitrypsin deficiency
the alveoli, alveolar ducts, and bronchioles
lower lobes
difference between bronchiectasis and COPD?
COPD: irreversible constriction
Bronchiectasis: irreversible dilation
what are the 2 components of pathogenesis for bronchiectasis
infection and obstruction
