RESPIRATORY SYSTEM

 

TUBERCULOSIS

 

 Within one hour of reaching the lungs, the bacilli are captured by the lymph nodes at the hilum and neutrophils begin phagocytosis. 

 

Then macrophages take over and 4 weeks later T-cell mediated immunity takes over forming a granuloma, in the centre of which there is necrotic caseation of bacilli.

 

After central caseation there is a concomitant rise in resistance and in the ability of inhibition of intracellular replication of tubercle bacilli.  Hence disseminated Miliary TB is very rare. 

 

Caseation heals with calcification and fibrosis.  Only when chronic ill health makes the immunity wane, reactivation in the lung may occur.  The caseated cavity ruptures or empties into the bronchus and is naturally drained.

 

A pleural Effusion may develop because of immunological reaction.  Removal of this fluid appears to be only psychologically beneficial as removal of 1-litre results in only less than 500 ml of lung volume expansion. 

 

BRONCHIAL ASTHAMA

 

 The allergen attaches to IgE antibody and this complex attaches to the mast cells and ruptures it, releasing lysozymes. 

 

Bradykinin, Serotonin, Histamine, Heparin and slow reacting substances of anaphylaxis, which cause bronchospasm and vascular congestion and oedema to reduce the antigenic input.  Eosinophils then migrate to the allergic tissues, after signals from the mast cells and detoxify the mediators and phagocytose the antigen antibody Cx. 

 

Increased mucus production occurs due to increased capillary permeability and plasma exudes out into the airway lumen and viscid balls of mucus are formed which are expelled out after the attack subsides. 

 

The specific IgE antibodies are produced for specific antigens.  40% of patients the attacks become less frequent and less severe and in 20% complete remissions can occur. 

 

The Endogenous corticosteroids increase four fold and block some of the inflammatory effects of the AgAb reaction without interfering with the immune complex destruction.  There is macrophage activation, release of TNF and IL’s, which triggers inflammation. 

 

The mild asthmas are managed by the mast cells and severe asthmas by the B-lymphocytes and IgE. 

 

There is T lymphocyte activation in addition which via CMI and cytokines increases the lifespan of eosinophils. 

 

Epithelial cells are shed and give easy access of inflammatory cells from capillaries to allergan in the airway and in addition epithelial cells release intercellular adhesion molecule.

 

ICAM-II, which captures the AgAb complex within the epithelial cell before being shed out. The nerve endings are exposed and Neuropeptides are released which in turn increase the permeability and mucus formation. 

 

Dr.Michael Abramson Monash University in Melbourne, Australia after studies on Asthmatics reports that high blood levels of salbutamol were  more than twice as high in dying patients than in surviving patients. 

 

IgE Antibodies to common environmental materials/pollutants are present in 30-40 % of population , many asymtomatic, this shows that a large majority overcome allergies by beneficial antibody response.

 

RESPIRATORY  FAILURE

 

Type I is hypoxic and Type II is hypercapnic (+ decreased PO2)

 

Various compensatory mechanisms exist, as outlined

 

(1) High output state by the heart.

 

(2) HCO3 retention by the kidney corrects the acidosis.

 

(3) Alterations in tidal volume, respiratory rate and changes in pressure of inspired air by use of accessory respiratory muscle are all dictated by the respiratory centre.

 

(4) In fact the condition of respiratory alternans denotes a breath to breath alteration in the relative contribution of intercostal muscles and the diaphragm.

 

(5) In ventilators volume, pressure, O2% and Resp rate can all be set by by passing the wisdom of the respiratory centre and in addition posing a problem of weaning from the ventilator as the patient has long forgotten how to breathe effectively on his own after the dependence on the ventilator.