BOOK BASED

Etiology: Precipitating Factors

Predisposing Factors: Tubercle Bacilli
(Mycobacteriu Repeated close contact with infected
 Immune compromised status m tuberculosis) persons

Etiology:
Mycobacterium
tuberculosis

Inhalation of mycobacteria & becomes

infected

Tubercle bacilli invasion in the apices

of the lungs or near the pleurae of
the lower lobes

Bacteria transmitted through airways

to the alveoli

Deposit and multiply

Bacilli transports via bloodstream or

Body: lymph systems to parts of: Areas of lungs:
Kidney, bones , Upper lobe
and central cortex

Inflammatory reaction: TB specific

Inflammatory reaction: Phagocytes
lymphocyte lyse bacilli and alveolar
engulf many of the bacteria
tissue
 Granulomas surrounded by Tissue reactions results in
macrophages which forms accumulation of exudate in alveoli
protective wall

Transformed into fibrous tissue

mass

Material (bacteria & macrophage)

become necrotic Accumulation of
exudates in alveoli

- fever and chills

Cheesy mass calcifies and forms - productive cough - sweating
collagenous scar - phlegm - loss of appetite
- weight loss

Bacteria is dormant, no further PRIMARY INFECTION

progression of active disease (Occurs 2-10 weeks after
exposure)

Reinfection

Reactivation of dormant
bacteria

SECONDARY INFECTION

Compromised Immune
System

Active Disease

Ghon tubercle hemoptysis

ulcerates

Heals and forms scar Releasing the cheesy

tissue material into the bronchi
 Causes infected lung to Bacteria becomes
be inflamed airborne

Further development of: Infect Others

 Bronchopneumonia
 Tubercle Formation

Spread in hilum of lungs Spread of the disease

then in adjacent lungs

Severe occurrence of lesions Accumulation of

in the lungs leading to abscess pus in the chest
cavity
(empyema)

Lung consumption
- fever and chills
- excessive sweating
↓ alveolar tissue - loss of appetite
leading to ↓ oxygen - weight loss

DEATH

TB begins when a susceptible person inhales mycobacteria and becomes infected. The
bacteria are transmitted through the airways to the alveoli, where they are deposited and begin
to multiply. The bacilli also are transported via the lymph system and bloodstream to other parts
of the body (kidneys, bones, cerebral cortex) and other areas of the lungs (upper lobes). The
body’s immune system responds by initiating an inflammatory reaction. Phagocytes (neutrophils
and macrophages) engulf many of the bacteria, and TB-specific lymphocytes lyse (destroy) the
bacilli and normal tissue. This tissue reaction results in the accumulation of exudate in the
alveoli, causing bronchopneumonia. The initial infection usually occurs 2 to 10 weeks after
exposure.
Granulomas, new tissue masses of live and dead bacilli, are surrounded by
macrophages, which form a protective wall. They are then transformed to a fibrous tissue mass,
the central portion of which is called a Ghon tubercle. The material (bacteria and macrophages)
becomes necrotic, forming a cheesy mass. This mass may become calcified and form a
collagenous scar. At this point, the bacteria become dormant, and there is no further
progression of active disease.
After initial exposure and infection, active disease may develop because of a
compromised or inadequate immune system response. Active disease also may occur with
reinfection and activation of dormant bacteria. In this case, the Ghon tubercle ulcerates,
releasing the cheesy material into the bronchi. The bacteria then become airborne, resulting in
the further spread of the disease. Then, the ulcerated tubercle heals and forms scar tissue. This
causes the infected lung to become more inflamed, resulting in the further development of
bronchopneumonia and tubercle formation.
Unless this process is arrested, it spreads slowly downward to the hilum of the lungs and
later extends to adjacent lobes. When severe occurrence of lesions in the lungs happens, it
leads to abscess which causes the accumulation of pus in the chest cavity (empyema). Now,
lung composition happens thus lead to alveolar damage making oxygen levels in blood
decrease which then in worst cases may cause inevitable death.
The process may be prolonged and is characterized by long remissions when the
disease is arrested, followed by periods of renewed activity. Approximately 10% of people who
are initially infected develop active disease. Some people develop reactivation TB (also called
adult-type progressive TB). The reactivation of a dormant focus occurring during the primary
infection is the cause.
The signs and symptoms of pulmonary TB are insidious. Most patients have a low-grade
fever, cough, night sweats, fatigue, and weight loss. The cough may be nonproductive, or
mucopurulent sputum may be expectorated. Hemoptysis also may occur. Both the systemic and
the pulmonary symptoms are chronic and may have been present for weeks to months
(Brunner’s Textbook of Medical-Surgical Nursing, 2017)

PATIENT BASED
Etiology: Precipitating Factors:
Predisposing Factors: Tubercle Bacilli Exposure to PTB patients in hospital
(Mycobacteriu visits
 Immune compromised status m tuberculosis) Occasional smoker and drinker
due to old age

Etiology:
Mycobacterium
tuberculosis

Inhalation of mycobacteria & becomes

infected

Tubercle bacilli invasion in the apices

of the lungs or near the pleurae of
the lower lobes

Bacteria transmitted through airways

to the alveoli
 Deposit and multiply

Bacilli transports via bloodstream or

lymph systems to parts of: Areas of lungs:
Upper lobe

Inflammatory reaction: TB specific

Inflammatory reaction: Phagocytes
lymphocyte lyse bacilli and alveolar
engulf many of the bacteria
tissue
Granulomas surrounded by Tissue reactions results in
macrophages which forms accumulation of exudate in alveoli
protective wall

Transformed into fibrous tissue

mass

Material (bacteria & macrophage) Accumulation of

become necrotic exudates in alveoli

- fever and chills

Cheesy mass calcifies and forms - productive cough - sweating
collagenous scar - phlegm - loss of appetite
- weight loss

Bacteria is dormant, no further PRIMARY INFECTION

progression of active disease (Occurs 2-10 weeks after
exposure)

Reinfection

Reactivation of dormant
bacteria

SECONDARY INFECTION

Compromised Immune
System
 Active Disease

Ghon tubercle hemoptysis

ulcerates

Heals and forms scar Releasing the cheesy

tissue material into the bronchi

Bacteria becomes
airborne

Infect Others

Spread of the disease

The patient’s causative agents that contribute to pulmonary tuberculosis are divided into
two (2), first is the predisposing factor which is the immune compromised status of the patient
due to old age. Because of the compromised immune status of the patient, it only means that he
is likely to get infections more frequently than most other people, especially airborne. As
mycobacterium tuberculosis is an airborne infection, the transmission is rapid. On the other
hand, the precipitating factors includes the exposure to PTB patients in hospital visits and being
an occasional smoker and drinker. First, being exposed to PTB patients in hospital visits have a
great factor, as said earlier, pulmonary tuberculosis caused by mycobacterium tuberculosis is
an airborne and anyone that inhaled this becomes infected. While being an occasional smoker
also contributes to acquiring PTB, the main reason is because cigarettes damage the lungs and
impacts immune system making the patient more susceptible to the said infection. Meanwhile,
alcohol consumption impairs the immune system, akin to smoking it also increases the patient’s
susceptibility to tuberculosis infection.
Once inhalation of mycobacteria happens and infection occurs, the bacteria begin
invasion in the apices of the lungs which is transmitted through the airways into the alveoli.
Once mycobacterium bacilli is in there, they are deposited and starts to multiply. This bacilli then
transports via bloodstream or lymph nodes to the upper lobes of the lungs which then triggers
the body’s inflammatory response which includes the TB specific lymphocyte that lyse the bacilli
and alveolar tissue, and the phagocytes that engulf many of the bacteria. In former, tissue
reactions result in accumulation of exudates in alveoli which then is the reason why productive
cough and phlegm forms. While in latter, granulomas are surrounded by macrophages which
then forms a protective wall then again transformed into fibrous tissue mass. The materials
which are bacteria and macrophages, becomes necrotic thus cheesy mass like forms. Once
cheesy mass calcifies and forms collagenous scar, productive cough and phlegm also forms.
Fever and chills, excessive sweating, loss of appetite, and weight loss are the most common
signs and symptoms of primary infection. Now, the bacteria become dormant, and no further
progression of active disease is happening.
Reinfection and reactivation of dormant bacteria because of exposure and compromised
immune system contributes to secondary infection in which now we call the active disease. In
this, Ghon tubercle ulcerates which hemoptysis occurs in which this is the time where the
patient spitted blood together with the cough. Also, once Ghon tubercle ulcerates it releases the
cheesy material into bronchi which makes the bacteria becomes airborne and that increases the
chances of the patient infecting others and spreading the said disease. This ulcerate will heal
and form scar tissue. If TB treatment is successfully implemented then the discomfort that the
patient is experiencing would alleviate a lot, however lung damage like cavities will still be there.

Wilkins, L. W. (2017). Brunner’s Textbook of Medical-Surgical Nursing 14th Edition + Lab

Handbook Package (14th ed.). LWW.