2. Pulmonary tuberculosis
(Phthisis)
This is a disease of lungs, pleurae or mediastinal lymph
nodes caused by mycobacterium tuberculosis.
The infection occurs in about 20% to 43% of the world
population.
About 3 million people all over the world die of this disease
every year.
Infection occurs in a susceptible person by air bourn
(droplet) infection.
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3. Predisposing factors
Age: all ages but highly susceptible below 3 years,
particularly in infancy.
Devitalised conditions: chronic malnutrition, diabetes,
HIV infection avitaminosis, famine(extreme scarcity of
food) etc.
Economic status: common in poor communities due to
poverty, immigration, poor sanitation, housing state,
nutrition & overcrowding, etc.
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4. Genetic factors: host resistance may be lowered by
genetic factors.
Addiction to tobacco, smoking etc.
Occupational diseases: silicosis, asbestosis
Causative organism: two species- M. tuberculosis & M.
bovis affect the human race
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6. Pathology
Tubercle bacilli get entrance into the human body through various
routes e.g. respiratory, GI, cutaneous & other. When the subject(usually
a child) is exposed to a diseased individual via droplet infection the
organisms enter the respiratory tract commonly.
Because of adequate ventilation, lower two third of lungs is the
common place of lodgement of the organism.
In most subjects with intact cell mediated immunity the organisms are
surrounded by macrophages & T cells which limit their multiplication
& spread.
This stage is called primary Tb which can not be clinically suspected or
radiologically detected.
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7. They are also engulfed by the macrophages, and are
affected by the biocidal property of the macrophages.
In this way viable tubercle bacilli may remain dormant for
even 20 years, or more within the granuloma.
In latent(hidden) tuberculosis there is no active disease &
hence transmission of the organisms to other individuals is
not possible.
In conditions of diminished defensive mechanism or
immunity active Tb may develope in about 5% to 10% of
cases about 2 years after.
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8. Increased risk of reactivation of Tb occurs in-
1) Diabetes
2) Chronic malnutrition
3) Immunosuppression: HIV infection, steroid therapy
4) Gastrectomy
5) Silicosis etc.
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9. The characteristic tissue reaction develops anywhere
according to the site of lodgement of the organisms.
This is called tuberculous granuloma which consists of
(from within outwards):
a) Central necrotic area unergoing caseation(firm, dry mass
like cheese in appearance)
b) Epetheloid & macrophage cells.
c) Langhans type of giant cells
d) Lymphocytic barrier at the periphery containing T.
lymphocytes.
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10. Primary pulmonary Tb
Pathogenesis & pathological changes:
When the child is exposed to a diseased individual, via droplet infection the
organisms enter the respiratory tract commonly .
Because of adequate ventilation, lower two-thirds of the lungs are the common
sites for lodgement.
The organisms are ingested(swallowed) by macrophages; their organisms either
die or multiply, and ultimately are carried to the regional lymph nodes & then
to other organs of the body through blood stream before specific immunity
develops.
During this period as they produce no toxin so no general reaction, and
no symptoms are present.
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11. Afterwards, the characteristic tissue reaction develops anywhere according to
the site of lodgement of the organism.
This consists of central necroting area undergoing caseation, epitheloid cells,
Langhans type of giant cells and a lymphocytic barrier at the periphery. This is
the characteristic lesion of tuberculosis.
When caseation develops, this is associated with liberation of various cytotoxic
materials from T lymphocytes giving rise to marked reduction in the
population of the organism.
At the same time those toxic materials destroy the parenchymal tissue of the
host.
After this, the process of primary infection gradually withers away & closed up
by a process of healing by fibrosis, calcification, etc.
Incubation period: 4-8 weeks
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12. When healing takes place by calcification, pulmonary
component can be seen as an opaque subpleural spot
on X-ray & it is called Ghon’s focus.
When supleural focus & hilar lymph nodes both are
calcified it is called Ranke’s complex.
When hilar lymph nodes are enlarged they may press
the bronchus giving rise to collapse of the lung
particularly of the right middle lobe. This is called
middle lobe syndrome.
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13. Clinical types with feature
Asymptomatic type: commonest type, 75-80% of all cases, Ghon’s focus on X-
ray & positive mantoux test(a test for immunity to tuberculosis using
intradermal injection of tuberculin) are evidence of past infection.
Febrile type: in some cases the only manifestation is fever ranging from (1000-
1030 F) lasting for 1-2 weeks. WBC count is normal but ESR remains high.
Allergic type: patient may show erythema nodosum or phlyctenular
keratitis(corneal infection), conjunctivitis or both. Some times there may be
allergic bronchospasm.
Progressive type: (5%) patient may develop tuberculous pneumonia,
bronchopneumonia, pleurisy, pleural effusion, miliary tuberculosis,
tuberculous meningitis, lobar or segmental collapse or even post primary Tb.
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14. Investigations
1. Mantoux test shows a positive reaction.
2. Sputum examination for AFB is usually negative.
3. Chest X-ray(PA) may show enlarged hila nodes with
subpleural lesion. There may be pleural effusion or
atelectasis.
4. ESR is raised.
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15. Acute miliary Tb
Pathogenesis:
Hilar lymphadenopathy occurs in cases of primary Tb. In course of
time these lymph nodes become caseous & softened & ultimately these
softened materials are poured into a near by pulmonary venule or
arteriole as its wall is thin.
If these are poured into a venule, the infected material is disseminated
throughout the body & this is called generalised miliary Tb.
When these materials enter an arteriole, only pulmonary
dissemination occurs according to the segmental distribution of the
pulmonary arteriole. This is called pulmonary miliary Tb.
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16. Each localised lesion resembles millet seed(ragi/mandia)
in appearance & therefore the disease is called miliary Tb.
Microscopic picture:
Each localised lesion reveals the following from within
outwards:
a) Central necrotic area without caseation
b) Scanty or no giant cells
c) Few lymphocytes
d) Least vascular reaction
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17. Clinical features
Onset is usually sudden, rarely insidious which is seen in middle aged & elderly
individuals.
Symptoms:
1. Fever: high remittent or intermittent type
2. Headache
3. Severe sweating
4. Cough-less prominent
5. Dyspnoea
6. Anorexia, weakness & emaciation
7. Convulsive seizure
8. Gradually unconsciousness sets in.
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18. O/E:
General survey:
Age- children
Sex- both
Pulse- tachycardia
RR- hurried
Central cyanosis- may be present
Emaciation- present
Patient may be toxic, delirious and unconscious
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19. Respiratory system: chest sounds are usually nil but sometimes widespread
crepitations are heard.
Nervous system: patient may be comatose. Slight neck rigidity is present.
Kernig’s sign(indicate subarachnoid hemorrhage or meningitis) is present.
Jerks are dull.
Choroidal tubercles seen in opthalmoscopic exam.
Alimentary system: abdomen may be bloated. Spleen may be palpable, soft &
tender. Liver is also enlarged, soft & tender.
According to the involvement, the disease may also be clinically classified into-
a) GI or enteric type
b) Respiratory or pulmonary type
c) Neural or meningitic type
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20. Investigations
Blood shows slight leucocytosis, high ESR
Mantoux test may sometimes be negative due to anergy(absence of
the normal immune response to a particular antigen or allergen).
Chest X-ray(PA) show bilateral snowstorm or millet seed appearance
with remarkable absence of vascular markings. Hilar lymphadenopathy
may be present.
Sputum is usually negative for AFB.
CSF may reveal features of tuberculous meningitis in late stages.
Biopsy of liver, bone marrow or lymph node may show tuberculous
granuloma.
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21. Prognosis
If not treated with
antitubrculous drugs
death takes place within
weeks from tuberculous
meningitis or respiratory
failure.
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22. D/D
Enteric fever: temp is continued, step ladder type, more in
evening, but not high swinging in type, choroidal tubercles
are absent, blood test show leucopenia, positive blood
culture. Widal reaction is also positive after 7 days of fever.
No miliary shadow in chest X-ray.
Septicaemia: patient is very toxic, a primary source of
septic focus may be found anywhere in the body; blood test
shows lecocytosis; blood culture is positive. Chest X-ray is
negative.
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23. Acute lobar pneumonia: patient is dyspnoeic & toxic
from the very beginning. Haemoptysis. Pulse respiration
ratio is altered. Chest shows, localized findings of
consolidation. Sputum is positive for specific organism.
Chest X-ray show pneumonic lesion.
Infective endocarditis: anaemia, clubbing, Osler’s
nodes(red-purple, slightly raised, tender lumps found in
fingers), splenomegaly, cardiac lesion, embolic
manifestations are present. Blood culture will show the
growth of streptococcus viridans usually.
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24. Acute B. Coli pyelonephritis: temp is high swinging in
type associated with chill & rigour, frequency of
micturition is present, toxaemia is little, loin & renal
regions are extremely tender, blood shows leucocytosis,
urine shows plenty of pus cells, RBC & organisms.
Empyema & subdiaphragmatic abscess: X-ray & USG
will help in the diagnosis. When pus somewhere is
suspected but its existence is not identified,
subdiaphragmatic abscess should be suspected. So there is
a common saying “pus somewhere, pus no where, pus is
under the diaphragm”.
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25. Histoplasmosis, Coccidioidomycosis, Blastomycosis,
Cryptococcosis
They can also produce identical clinical picture &
should be differentiated from acute miliary
tuberculosis
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26. Post primary tuberculosis
(Adult phthisis)
Post primary tuberculosis occurs:
a) Directly from a primary lesion,
b) From reactivation of primary lesion(Simon’s focus)
or
c) Re-infection after the primary lesion has been
completely healed up.
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27. Pathogenesis
It begins as a small caseopneumonic focus in apical &
posterior segment of the upper lobe or apical portion of the
lower lobe, the focus is called early infiltration.
Patient with HIV infection with or without AIDS are at
increased risk of developing tuberculosis.
HIV infection is considered to be an important risk factor
for development of Tb in the developed, developing &
underdeveloped countries.
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28. Clinical features
Constitutional symptoms: weakness, lassitude( lack of
energy), malaise(feeling of discomfort, illness), loss of weight,
loss of appetite, sweating at night, evening rise in temp,
palpitation, menstrual disturbances, rapid
emaciation(abnormally thin) etc.
Symptoms due to local affection of lung: cough, chest pain,
sputum, haemoptysis.
General survey: patient is emaciated, raised temp, tachycardia
even during sleep.
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29. Chest examination:
Inspection: flattening of chest on the affected side with
diminished movement. When the disease is localised to the
apical part of lung, Morenheime’s fossa(infraclavicular fossa)
becomes prominent.
Palpation: increased vocal fremitus; trachea & apex beat may be
in normal position
Percussion: there may be increased resonance
Auscultation: bronchial breath sound is present, vocal
resonance is increased, coarse crepitations are present.
Sometimes there may be post-tussic crepitations.
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30. Investigations
Bacteriological examination:
a) Sputum
b) Tracheo-bronchial washing
c) Gastric washing
Chest X-ray: infiltration, pneumonic shadow,
cavitation
Biopsy: FNAC, pleural & pulmonary biopsy
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33. Pleural fluid test in Tb associated with pleural effusion
Skin testing: Intracutaneous injection(Mantoux test) or
by multiple puncture method(thine test, Heaf test)
Blood: Shows normal, low & high leucocyte count. ESR is
usually high. These changes never help in diagnosis.
Serologic diagnosis: by ELISA(enzyme-linked
immunoassay to detect antibodies in the blood) technique
IgG antibody can be measured against mycobacterial
antigen.
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34. Management of Tb
Bed rest: till symptoms like fever, haemoptysis, etc.
persist. Sputum positive cases should be isolated till
they become negative as they cause rapid spread of
disease in the society.
High calorie, high protein diet supplemented with
vitamins.
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35. Drugs:
Antituberculous drugs divided into 3 groups:
Most potent drugs:
Isoniazid(INH), Rifampicin(RIF), Pyrazinamide(PZA),
Ethambutol & Streptomycin(SM)
Moderately potent drugs:
Ethionamide(ETA), Thiacetazone(THZ), Cycloserine(CS),
Capreomycin(CAP), Kanamycin(KM), Amikacin(AMK)
Potency unknown drugs:
Ciprofloxacin(CIPRO), Ofloxacin(OFLG)
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36. For newly diagnosed cases before starting therapy one
must inquire about the possibility of INH resistance by
following:
I. Was the patient treated with anti-Tb drugs before?
II. Does the patient belong to a country where the disease is
very much prevalent & drug resistance is common, e.g.
South-east Asia, Africa or Latin America?
III. Has the patient acquired infection from a drug resistant
case?
IV. Does the patient belong to an area where INH resistance
is common(>5%)
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37. When the answer to all the question is “no” patient
should be given:
1. INH 300 mg orally daily
2. RIF 450-600 mg orally daily before food
3. PZA 750 mg orally twice daily
4. Ethambutol 800 mgm/day.
All 4 drugs are to be continued for a period of 2
months.
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38. After 2 months :
INH & RIF are to be continued for 4 months more, in
same doses as before.
Total period of treatment varies from 6-9 months.
In no case less than 6 month therapy is recommended
as chance of relapse is more.
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39. Six month therapy is ended when sputum culture is
negative for 3 different consecutive days.
If PZA is not used in first 2 months then INH, & RIF should
be continued for 7 months that means total 9 months.
maximum duration of 9-12 months is considered only when
there is a break, non-compliance or slow response or with
single drug therapy. Life long therapy is never used.
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40. When the answer to all the question is “yes” the
following regime should be started until drug
susceptibility result is available.
(streptomycin)SM or (Capreomycin)CAP 0.5-1 gm IM
daily (5 days a week)
INH 300 mg, RIF 600 mg, PZA 30 mg/kg daily for 8
weeks when susceptibility result is available.
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41. (a) Sensitive to INH& RIF: therapy to be started as in “no”.
(b) Resistance to INH: RIF 600 mg, PZA 40-50 mg/kg, SM 20
mg/kg twice weekly for 7 months. INH 900 mg twice
weekly may be added if resistance permits.
(c) Resistance of INH & RIF: SM/CAP 0.5-1 gm IM/day(5
days a week), EBM(ethambutol) 25 mg/kg,
ETA(Ethionamide) 18 mg/kg, CS(Cycloserine) 18 mg/kg,
PZA 3 mg/kg for 1 ½ -2 years.
(d) Surgical: for localised chronic Tb with or without cavity,
surgical resection is to be considered.
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