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Respiratory > Lecture 12- Asthma > Flashcards

Lecture 12- Asthma Flashcards

1
Q

What is Asthma?

A

A chronic inflammatory disease of the airways, characterised by recurring symptoms, airflow obstruction and broncho spasm.
Variable episodic airflow obstruction: reversible either spontaneously or without treatment.

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2
Q

Asthma symptoms

A 
wheezing
coughing
Airflow obstruction
Dyspnea
sputum production
chest tightness
shortness of breath

These become worse at night-time

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3
Q

Asthma facts

A
  • very common chronic disease
  • 1/6 adults and 1/4 children
  • > 600,000 kiwis
  • > 500,000 kiwis take meds
  • $800M economic burden
  • most common cause of hospital admission in kids (hosp rates double in past 30 yrs)
  • More common in developed countries
  • YLD: 1st males and 3rd females
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4
Q

Is it more common in males or females? What age?

A

Adults : females more common
Kids: Males more common

Girls>boys
Highest in ages 18-44

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5
Q

Asthma can be..

A

Episodic: acute exacerbations interspersed with symptom-free periods
Chronic: daily AW obstruction which may be mild, moderate or severe AND acute exacerbations
Life Threatening: slow onset or fast-onset (fatal within 2 hours)

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6
Q

How would you Diagnose Asthma?

A

1) Physical examination: Wheezing (not specific to asthma)
2) History of: Recurrent wheeze, dyspnea, cough, chest tightness and reversible airflow limitation and diurnal variation
3) Lung Function test: evidence of variable airflow obstruction
4) Symptoms above worsen due to: exercise, animals with fur/feathers, dust-mites, moulds, smokes, pollen, weather change, laughing or crying excess
5) Other: family history, atopic disease (allergic rhinitis, urticaria or eczema)

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7
Q

Atypical Presentation

A
  • Dyspnea without wheezing
  • Chronic cough
  • Increased shortness of breath at nighttime
  • Allergic rhinitis with wheezing
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8
Q

Types of Lab studies done

A
  • Lung Function Tests
  • Skin allergy test and serologic studies
  • radiographic studies
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9
Q

Lung Function Tests

A

1) Peak Expiratory Flow (PEF): cheap, easy to do, useful to monitor treatment process but not good to diagnose as everyones so variable
2) Spirometry (FEV1): Better diagnostic tool, not suitable for young patients

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10
Q

Asthmatic Spirometry

A

Big drop: FEV1
Drop in : FVC
FEV1/FVC
Post-bronchodilator Reversibility testing: FEV1 increases (if > 400mL it’s likely you have asthma, a good distinguisher from COPD)

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11
Q

Serologic Studies

A

Eosinophil count:
>4% or 300-400/mm^3

> 800/mm^3 suggests the presence of other disorders

Increased Serum IgE level

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12
Q

Allergy Tests for

A 
Pollens
dust mites
mold and mold spores
animal Dander
Insect allergens
Smoking
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13
Q

What are the Two major models of Asthma

A

Allergy and non-allergy

Up to 90% of early-onset asthma could be allergic

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14
Q

Atopic (allergy) Asthma

A
  • Most common
  • usually early-onset
  • Triggered by environmental antigens
  • A positive family history
  • often preceded by allergic rhinitis, urticaria or eczema
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15
Q

Principle cells of Inflammation

A

Eosinophils: (late-phase)
Mast Cells: exercise-induced asthma and acute phase response
Macrophages: release pro-inflam mediators
T cells: central role in inflammation responses
Neutrophils: corticosterol resistance
Basophils: also in late-phase response to allergin exposure
Dendritic: Present allergin to inflamm cells

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16
Q

Appearance of asthma microslide

A

Changed SM and goblet cells, thicker BM, higher density of inflammatory cells and a damaged epithelial layer

17
Q

Types of response to an allergen challenge in atopic sufferers

A

1) Acute-Phase Response (APR): inhalation causes an immediate fall in lung function (~5-10minutes). Can sometimes be reversed w/o treatment
2) Late-phase response (LPR): Beginning about 4-6 hours after allergen challenge. Lung function lower and persistent
3) Dual phase

18
Q

Lung function journey of responses after an allergen challenge

A

1) Acute-Phase: drops to 50% within 30 mins, returns to normal within 2 hours
2) Late-Phase: post 4 hour drop to ~40%, takes around 20hrs to return
3) Dual-phase: lung function can be extremely bad (~30%) for 24hr

19
Q

Draw flow diagram page 12.9

A

…

20
Q

Genetic Involement of Asthma

A

~30 SNPs have been related to asthma, but nothing is certain

  • A genetic predisposition to Th2 rather then Th1
  • When a body decides to go down a Th pathway (decided by genes) it naturally inhibits the other pathway
21
Q

Th2 and Th1

A

Th1: produce IFN-y, IL-2 and TNF-alpha
Main cell partner is macrophage

Th2: secrete cytokines (IL-4, IL-5)
main cell partner is B-cell

22
Q

Th2 pathway

A

1) causes type 1 hypersensitivity/atopy: such as eczema, hayfever, asthma
2) Chronic airway inflammation
3) Bronchial hyper responsiveness

23
Q

Non-atopic Asthma

A
  • Majority is late-onset
  • Maybe associated with respiratory tract infections
  • other risk factors: medication induced asthma (NSAIDS, beta-blockers, aspirin)
24
Q

Key Mediators in asthma

A 
Leukotrienes
Prostanoids
Acetyl Choline
Chemokines
IgE
Nitric Oxide
Granule Proteins
Adhesion molecules in inflammation
25
Q

Leukotrienes

A
  • de novo synthesis of mast cells & eosinophils
  • Potent mediator (LTC4) causing prolonged broncho-constriction
  • increases mucus secretion + vascular permeability > edema
  • L receptor antagonists recomended as 2nd line of treatment
26
Q

Prostanoids

A
  • Produced by mast cells and eosinophils

- Potent bronchoconstrictors (PGD2)

27
Q

Acetyl Choline (ACh)

A
  • Release from intrapulmonary motor nerves
  • causes SM contraction in airways
  • stimulates muscarinic receptors
28
Q

Chemokines

A
  • recruit or chemotaxis of inflamm cells

- CK receptor inhibitors for CCr3 and CCR4 are in development for therapy

29
Q

IgE

A
  • Triggering mast cell
  • cause airway inflammation
  • humanized monoclonal AB targeting IgE is developed for therapy ‘Xolair’
30
Q

Nitric Oxide

A
  • Higher levels in Asthma
  • So production reflects level/severity of airway inflamm
  • Exhaled NP measurement used to monitor inflamm extent for asthma control
31
Q

Granule Proteins

A
  • Mast cells, basophils, neutrophils and eosinophils release them
  • MBP major basic protein
  • ECP eosinophil cationic protein
32
Q

Adhesion molecules

A

Integrins: primary mediators of cell-extracellular matrix adhesion
important for transendothelial migration of inflamm cells into airways

Respiratory (19 decks)

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