Pulmonary tuberculosis

PULMONARY TUBERCULOSIS

Risk factors –

• Close contact with sputum-smear positive
individual

Environmental factors that lower resistance –
Malnutrition, poor and overcrowded housing,
alcoholism and/ or drug addiction, heavy
smoking, corticosteroid therapy.

Relation to other disease – Not uncommon after
influenza, whooping cough. More common
with diabetes mellitus, cirrhosis of liver,
pneumoconiosis, and following partial
gastrectomy.

• Immunosuppression (including drugs and
autoimmune deficiency syndrome).

• HIV infection/ AIDS.
• Other risk factors – Kidney failure, diabetes,
silicosis, family history, IV drug abuser.

Route of infection – In majority by inhalation of air-
bone infected droplet nuclei derived from sputum of
an adult with cavitary pulmonary tuberculosis.

Clinical types:

  1. Primary pulmonary tuberculosis –
    Primary
    tuberculosis refers to events following invasion by
    tubercule bacillus infection, being commonly caused
    by inhalation (rarely through skin or ingestion) of the
    bacilli into the lungs.

Primary complex-
Inhaled bacilli are deposit
in the alveoli where a subpleural inflammatory lesion.

occurs. When they reach the regional lymph nodes,
these also become intected The tuberculin test
becomes positive within 6 weeks of the infection
These two components of the primary complex
resolve without complications and sometimes result
in local calcification.

Primary tuberculous infection calcified stage
PROGRESS- of primary complex may occur thus –

  1. Haematogenous dissemination – about 3 months
    after primary infection (a) Acute type – Miliary
    tuberculosis, T.B. meningitis. (b) Chronic type
  • with local manifestations in kidneys, bones,joints etc.

  1. Progress of lung component – most commonly in
    adolescents and young adults usually about 6
    months after initial infection. The lung focus
    extends, cavitates and pleural involvement
    leads to pleural effusion.
  2. Progress of lymph node component –
    It may cause pressure on trachea or main bronchi resulting in severe paroxysmal cough simulating whooping cough. There may also be dysponea, stridor or wheezing which may be mistaken for asthma.
  3. Bronchi involvement-(a) partial bronchial -obstruction with valve action causing obstructive emphysema (b) complete bronchial obstruction may result in large areas of homogeneous shadowing (formerly labelled epituberculosis). Bronchial involvement commonly involves middle lobes and upper lobes. Aspiration of infected material cause pneumonia or

collapse. Lesions may clear without sequelae
but sometimes result in permanent collapse,
bronchostenosis, bronchiectasis or
obstructive emphysema. (c) Middle lobe syndrome -the large middle lobe bronchus is particularly vulnerable and the bronchiectasis mY lead to recurrent middle lobe infection.

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