Bronchial asthma

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Transcript of Bronchial asthma

Bronchial Asthma

Dr.CSBR.Prasad, M.D.

Bronchial asthma - gist

Bronchial asthma

Disease characterized by increased

responsiveness of the tracheobronchial

tree to various stimuli, potentiating

paroxysmal constriction of the bronchial

tree.

Bronchial asthma Patients with asthma experience:

1. Attacks of severe dyspnea, coughing, and wheezing.

2. Rarely, “status asthmaticus” - may prove fatal.

3. Patients may be asymptomatic between the attacks.

In some cases, the attacks are triggered by exercise and cold or by exposure to an allergen, but often no trigger can be identified.

There has been a significant increase in the incidence of asthma in the

Western world in the past three decades.

In Bangalore 50% of children suffer from asthma. Air pollution is

thought to be the main culprit.

Definition

Chronic inflammatory disorder of airways that causes recurrent episodes of:

– Wheezing

– Breathlessness

– Chest tightness &

– Cough particularly at night and /or early morning

These symptoms are usually associated with wide spread but variable bronchoconstriction and air flow limitation that is at least partially reversible, either spontaneously or with treatment

It is thought that inflammation causes increase in airway responsiveness (bronchospasm) to a variety of stimuli

Frequency and severity of

symptoms

1. Mild, intermittent

2. Moderate

3. Severe, persistent

Clinical categories

1. Steroid dependent

2. Steroid resistant

3. Difficult

4. Brittle asthma

Informal categories

1. Seasonal

2. Exercise induced

3. Drug induced

4. Occupational asthma

5. Asthmatic bronchitis in smokers

6. Allergic bronchopulmonary aspergillosis

Typical categories

1. Extrinsic (allergic, reagin mediated, atopic)

2. Intrinsic (idiosyncratic)

3. Mixed (intrinsic and extrinsic factors

operative)

Figure 15-10 A simplified scheme of the system of type 1 helper T (TH1) and

type 2 helper (TH2) cells.

Structural alterations

“Airway remodelling”

• Smooth muscle proliferation

• Subepithelial collagen deposition

Mediated by:

1. Skewed TH2 differentiation

2. ADAM-33 gene abnormality

3. Mast cells

Figure 15-12

Comparison of a normal

bronchiole with that in a

patient with asthma.

Atopic / Allergic asthma

• Most common type

• Environmental agent: dust, pollen, food,

animal dander

• Family history - present

• Serum IgE levels - increased

• Skin test with offending agent –wheal flare

Two reactions

Classic Ig E mediated hypersensitivity

reaction has 2 responses

1. Acute immediate response

2. Late phase reaction

Figure 15-11 A model

for allergic asthma.

Pathogenesis

• Ag + presensitised IgE coated mast cells

to same or cross reacting antigen

• Chemical mediators

• Mucosal surface

• Submucosal mast cells

• Direct stimulation of subepithelial vagal

receptors

• Minutes – Bronchoconstriction.

Primary mediators

1.Th2 cells > IL 4,5 > IgE production+EØ &

Mast cell recruitment

2.Histamine - bronchconstriction by direct

and cholinergic reflex actions

3.ECF and NCF

Secondary mediators

LT C4, D4, and E4.

prolonged bronchospasm

increased vascular permeability

increased mucus secretion.

Prostaglandins (D2) Bronchospasm

Vasodilation

PAF platelet aggregation

granule secretion.

Late phase reaction starts 4-8hrs later and persits for 12-24hrs

Caused by recruitment of BØs, NØs, EØs

• HRF – Histamine releasing factor

• MBP – Major basic protein from EØs

Direct epithelial damage

• Neutrophils – inflammatory injury.

Non atopic asthma

• Triggered by respiratory tract infection

• Viruses - most common culprits

• Family history uncommon

• IgE level normal

• No associated allergy

• Skin tests NEGATIVE

• Cause- hyperirritability of bronchial tree.

Drug induced asthma

• Several pharmcologic agents

• Aspirin sensitive asthma

occurs in recurrent rhinitis

nasal polyposis.

• Increased bronchoconstrictor leukotrienes. Exqusitively sensitive to small doses of aspirin.

• Inhibits COX pathway, without affecting LPO pathway

Allergic Bronchopulmonary

Aspergillosis

• Caused by spores of aspergillus fumigatus

• Antigen challenge

• Type I IgE induced reaction

• 4 to 6 hr later Type III mediated response.

Occupational asthma

• Fumes (epoxy resins, plastics)

• Organic / chemical (dust, wood, cotton)

• Gases (toluene)

• Other chemicals (formaldehyde, penicillin)

• Mechanism of injury:

type I IgG mediated reactions

liberation of bronchoconstrictors directly

unknown hypersensitivity.

Morphology - gross

• Lungs, over distended due to over inflation

• Small areas of atelectasis

• Occlusion of bronchi and bronchioles by

thick tenacious mucous plugs.

These lungs appear essentially normal, but are the hyperinflated lungs of

a patient who died with status asthmaticus.

This cast of the bronchial tree is formed of inspissated mucus and was coughed up by a

patient during an asthmatic attack. The outpouring of mucus from hypertrophied

bronchial submucosal glands, the bronchoconstriction, and dehydration all contribute to

the formation of mucus plugs that can block airways in asthmatic patients.

Morphology - Micro

• Mucous plugs-whorls of shed epithelium

CURSHMANN’S SPIRALS

• Numerous Eøs and

CHARCOT-LEYDEN CRYSTALS

• Crystalloids made of MBP.

Microscopy (Airway remodeling)

• Thickening of BM of bronchial epithelium

• Edema and infammatory infiltrate in

bronchial walls with EØ (5 to 50 % )

• Increased in size of submucosal mucous

glands

• Hypertrophy of bronchial wall muscle.

Walk thru wheeze ?

Walk thru angina ?

E N D

Contact:

Dr.CSBR.Prasad, M.D.,

Associate Professor,

Deptt. of Pathology,

Sri Devaraj Urs Medical College,

Kolar-563101,

Karnataka,

INDIA.

CSBRPRASAD@REDIFFMAIL.COM