PULMONARY TUBERCULOSIS

(Koch’s Disease/Phtisis/Consumption Disease)

Pulmonary Tuberculosis Tuberculosis is a chronic, sub-acute or acute respiratory
disease commonly affecting the lungs characterized by the formation of tubercles in the
tissues which tend to undergo caseation, necrosis and calcification. It is caused by
Mycobacterium tuberculosis which is a gram-positive, acid-fast aerobic bacillus and can
be killed by heat, sunshine, drying and ultraviolet light. It resides in the sputum of
humans. The portal of exit from humans is through the mouth and nose (such as when an
infected person coughs, sneezes, sings or talks). A large number of this microorganism
escapes from the reservoir via the droplet nuclei which is the residue of the droplets from
coughing or sneezing that remains suspended in the air. It can be inhaled by other humans
who came in contact with it. Therefore the portal of entry of the bacilli to the host is
through the respiratory tract. The incubation period is from 2-10 weeks.
Period of Communicability
The patient is capable of discharging the organism all throughout life if he remains
untreated. The disease is highly communicable during its active phase.
Mode of Transmission
 The disease is transmitted by deliberate inoculation of microorganism or by droplet
 The disease is transmitted through inhalation of organism directly into the lungs
from contaminated air.
 It can also be transmitted through direct or indirect contact with infected persons,
usually by discharges from the respiratory tract by means of coughing,sneezing or
kissing
 The disease is transmitted through contact with contaminated eating or drinking
utensils
 Rarely can the disease be transmitted through skin lesion
Clinical Manifestations
 Afternoon rise of temperature
 Night sweating
 Body malaise and weight loss
 Dyspnea, hoarseness of voice
 Hemoptysis- considered as the pathognomonic sign of the disease
 Cough, dry to productive
 Occasional chest pains
 Sputum positive for AFB
PRIMARY INFECTION
 Change in behavior from normal to listlessness
 Easy fatigability
 Normal activity to irritability
 Crepitant rales
POST PRIMARY/PROGRESSIVE PRIMARY TB
 Appears visibly ill
 Cough gradually becomes distressing
 Increased breath sounds with audible fine crepitant rales
 Dyspnea
 Hemoptysis in those with cavitary disease
CHRONIC PTB - generalized systemic signs and symptoms
 General malaise, anorexia, easy fatigability, apathy, irritability, indigestion,
general influenza-like symptoms
 physical signs – tachycardia, low BP, dyspnea, cyanosis
 fever
 night sweats – occurs in cases with acute exudate involvement
CHRONIC PTB
- Pulmonary s/s:
 cough with mucoid or mucopurulent sputum
 fine crepitant rales at apical area during deep breathing
 hemoptysis and chest pain
 pleural pain with serofibrous pleurisy
 dyspnea
INCIDENCE
Tuberculosis (TB) is one of the top 10 causes of death worldwide. In 2015, 10.4
million people fell ill with TB and 1.8 million died from the disease (including 0.4
million among people with HIV). The largest number of new TB cases occurred in
Asia, with 61% of new cases, followed by Africa, with 26% of new cases
(WHO,2015).

RISK FACTORS
Close contact with someone who has active TB. Inhalation of airborne nuclei from
an infected person is proprtional to the amount of time spent in the same air space, the
proximity of the person, and the degree of ventilation
immunocompromised status. People with lowered resistance has a higher chance in
acquiring disease.
Living in overcrowded, substandard housing. Living in crowded places increases the
possibility of transmitting the disease from one family member to other.
Occupation. Being a health care worker performing high risk activities increases the
risk in acquiring disease sich as tuberculosis. Those also whose occupation includes
hardworking and vigorous work increases are classified to be risk in acquiring TB.
PATHOPHYSIOLOGY
Readings
PRIMARY INFECTION
After the bacilli gained entry to the host, it will pass down the bronchial tree and
implant themselves on the respiratory bronchioles or alveoli wherein oxygen is at highest.
Upon settlement in the alveolar space the Mycobacterium tubercle will initiate an
immediate acute inflammatory response by attracting alveolar macrophages and other
acute inflammatory cells like neutrophils. Due to the glycolipid capped mannose on the
mycobacteria, the macrophages will detect it as an antigen and start to engulf it. Upon the
engulfment of the MTB, macrophage is now susceptible to endosomal manipulation in
which the mycobacterium will conduct maturation arrest, neutralization of lysosomal
acidic pH and ineffective fusion of lysosome with phagosome thus it will lead to the
ineffective digestion of MTB and allow MTB multiplication inside the alveolar
macrophage. Although some alveolar macrophages may resist endosomal manipulation
through a genetic polymorphism which involves a protein called Natural Resistance
Associated Macrophage Protein 1 (NRAMP1). This kind of macrophages are capable of
digesting the mycobacterial antigen and present the antigen in the Major
Histocompatibility Complex. The MHC will then be recognized by the t-cells and the
macrophage will in turn release IL-12 to initiate the production of T-cell subtype which is
the Helper T-cell type 1 (TH1). TH1 will be produced in 3 weeks and will initiate a
delayed hypersensitivity response. B cells starts to produce an antibody against the
mycobacteria. (only after this, any exposure towards mycobacterial antigen will produce
a positive result for mantoux test).
On the other hand, as the MTB multiplies intracellulary to a point where the
macrophage cannot hold, it will eventually burst allowing MTB to escape. In order to
settle down and confine the infection, TH1 will produce interferon gamma to activate
alveolar macrophage into epitheloid cells. This epitheloid cells will in turn produce an
extensive amount of Tumour Necrosis Factor (TNF) in order to recruit more monocytes
from the circulation. The recruited macrophages will fuse together to form a larger
phagocytic cell called the Langerhan type giant cell. The accumulation of inflammatory
cells and a ring of fibroblasts will confine the infection in a granuloma. Consequent to
that, IL-1 which is known to be an endogenous pyrogen will be released as soon as
possible to stimulate the thermostat of the brain at the Organum Vasculasum of Lamina
Terminalis to increase the level of body temperature. By increasing the body’s
temperature, iron serum level will drop significantly and this will immobilize bacterial
growth as most bacteria need iron for replication. Therefore, at the early stage of
pulmonary TB, patient is presented with intermittent low grade fever.
DORMANT STAGE
After the confinement of the MTB in the granuloma , many macrophages die
releasing the tubercle bacilli and forming a caseous center in the tubercle. The aerobic
tubercle bacilli do not grow well in this environment but many remain dormant and serve
as a basis for later reactivation of the disease. However, this depends on the immune
status of the patient.
PRIMARY INFECTION (IMMUNOCOMPETENT)
For immunocompetent patients there are two possible events that may happen when
they encounter primary tuberculosis. First, because their immune system is so intact, the
whole mycobacteria are completely eradicated from the body. This kind of patient is still
susceptible to have a secondary infection if they go to highly densed contagious area but
it will only leave a scar due to fibrosis. Second possibility is that despite of the intact
immune system, some mycobacteria remain dormant inside the alveolar macrophage
without duplication and becoming infectious.
PROGRESSIVE PRIMARY TUBERCULOSIS (IMMUNOCOMPROMISED)
For the immunocompromised patients, they are incapable of fighting a primary
infection of MTB. Therefore, the infection can easily progress into a severe form of
infection called the progressive primary tuberculosis (PPT). It is characterized by the
formation of massive lesions without granuloma extending now the damage to a greater
area of the lungs which may result to various pulmonary complications. Due to the lack
of immunity, the bacilli tend to be transmitted through the lymphatic channels to the
regional lymph nodes causing now lymphagenitis and lymphadenopathy. With the
involvement of this lymph nodes to the primary infection, it is now called a ghon
complex or primary complex. In progressive primary tuberculosis, the ghon tubercle is
not confined in a granuloma thus, it can spread freely. The mycobacterium tubercle may
indirectly enter the bloodstream through the lymphatic circulation which empties into the
subclavian vein through the thoracic duct. The entry of the bacilli into the bloodstream
may cause extrapulmonary tuberculosis.
SECONDARY TB (IMMUNOCOMPETENT—IMMUNOCOMPROMISED)
In time, the previously sensitized patients can experience secondary pulmonary
tuberculosis due to reactivation or reinfection. Upon reactivation or reinfection, both will
initiate a tremendous inflammatory response with respect to the presensitized immune
system, leading to massive infiltration of inflammatory cells, production of numerous
granulomas with a classical caseation at the center. The disease progresses as the
caseous center now enlarges and caseous matter undergoes liquefaction allowing it to
spill out and spread to other areas of the lungs. Rales are heard upon auscultation due to
the fluid along the airway passage. The spillage also leaves an air-filled tuberculosis
cavity, an environment in which the aerobic bacilli favors to multiply.
Secondary tuberculosis causes uncontrolled inflammatory response which leads to
massive tissue destruction. This results to the inflammation along the pulmonary tract,
blood vessels surrounding the affected areas engorge due to the presence of inflammation
making them highly susceptible to destruction. When the blood vessels around the area
rupture, hemoptysis occurs.
Lung function becomes compromised due to the massive destruction of the
pulmonary parenchyma. In addition to this, fibrosis also occurs as a part of the healing
process and this further leads to lung function impairment. Since the patient is at a state
of hypoxia due to the compromised lung function, total body metabolism depletes
insidiously causing an easy fatigability. As a compensatory mechanism, the patient will
experience dyspnea in an attempt to increase the oxygen partial pressure inside the
systemic circulation.

DIAGNOSTIC PROCEDURES
 Tuberculin Skin Test (Mantoux Test)
 This is a standardized, intracutaneous injection procedure used to determine
whether a person has been infected with the TB bacillus and should be
performed only by those trained in its administration and reading
 Tubercle bacillus extract (tuberculin), purified protein derivative (PPD), is
injected in the intradermal layer of the inner aspect of the forearm,
approximately 4 inches below the elbow. Intermediate-strength PPD, in a
tuberculin syringe with a half-inch 26-or 27-gauge needle, is used
 The needle with the bevel facing up, is inserted beneath the skin. Then, 0.1 mL
of PPD is injected creating an elevation in the skin,, a well-demarcated wheal
6-10 mm in diameter
 The site, antigen name, strength, lot number, date and time of the testare
recorded
 The test result is read after 48 to 72 hours after injection
  The size of the induration (hardening) determines the significance of the
reaction.
Size Reading
0-4 mm Not significant
5 mm or > Significant in people who are considered to be at risk
Defined as positive in patients who are:
 HIV positive or have HIV risk factors and are of
unknown HIV status
 Close contacts of someone with active TB
 Have chest x-ray results consistent with TB
10 mm or > Significant in people who have normal or mildly
impaired immunity

 A significant (postive) reaction does not necessarily mean that active disease is
present in the body. However, all significant reactors are candidates for active TB.
The more intense the reaction, the greater the likelihood of an active infection
 A nonsignificant (negative) skin test does not exclude TB infection or disease,
because patients who are immunosuppressed cannot develop an immune response
that is adequate to produce a positive skin test (referred to as anergy)
 Blood Test
 Sputum Culture
PHARMACOLOGIC MANAGEMENT
 Pulmonary TB is treated primarily with anti-TB agents for 6-12 months. A prolonged
treatment duration is necassary to ensure eradication of the organisms and to prevent
relapse
TB Interferon Gamma Release Assays (IGRAs)
 Blood tests that measure a person’s immune response to the bacteria that cause
TB. The immune system produces some special molecule called cytokines. These
TB tests work by detecting a cytokine called the interferon gamma cytokine
 Results can be available within 24 hours, and prior BCG vaccination does not
cause a false positive result
Sputum smear microscopy
 Smear microscopy of sputum is often the first TB test to be used in countries with
a high rate of TB.
 In this test, a sample of sputum is usually collected by the person coughing. A
very thin layer of the sample is placed on a glass slide (smear). A series of special
stains are then applied to the sample, and the stained slide is examined under a
microscope for signs of TB bacteria
o Fluorescent microscopy
 The use of this test makes sputum TB tests more accurate. With a
fluorescent microscope, the smear is illuminated with a quartz
halogen or high pressure mercury vapour lamp, allowing a much
larger area of the smear TB to be seen and resulting in more rapid
examination of the specimen
Chest X-ray
 If a person has had TB bacteria which have caused inflammation in the lungs, an
abnormal shadow may be visible on a chest x-ray

PHARMACOLOGIC MANAGEMENT
1) Generic Name: Rifampicin
Classification: Antituberculars
Mechanism of Action: This drug inhibits RNA synthesis by blocking RNA
transcription in susceptible organisms thus, inhibiting multiplication
Therapeutic Effect: Bactericidal action against susceptible organisms
Dosage,Route,Frequency:
 Adults
PO  600 mg/day or 10 mg/kg/day (up to 600 mg/day) single dose , may also be
given 2-3 times weekly
 Children
PO  10-20 mg/kg/day single dose (not to exceed 600 mg/day); may also be
given 2-3 times weekly.
 Nursing Interventions Rationale
1) Administer medication on an empty To ensure absorption of drug
stomach at least 1 hour before or 2 hours after
meal with a full glass (240 mL) of water. If GI
irritation becomes a problem, may be
administered with food

2) Advise patient to take medication once daily To ensure therapeutic and prevent resistance
(unless biweekly regimens are used), as
directed, and not to skip doses or double up on
missed doses. Emphasize the importance of
continuing therapy even after symptoms have
subsided

3) Advise patient to notify health care

professional promptly if the following These are signs and symptoms of hepatitis
happens:
 Jaundice
 Vomiting
 Anorexia
 Unusual tiredness
 Weakness
4) Caution patient to avoid the use of alcohol This may increase the risk for hepatotoxicity
during the therapy
5) Advise patient to avoid activities that This drug may cause drowsiness
require mental alertness
6) Inform patient that saliva, sputum, sweats, To prevent anxiety
tears, urine, and feces may become red-orange
or red-brown
 2) Generic Name: Isoniazid
 First line therapy of active tuberculosis, in combination with other agent
Classification: Antitubercular
Mechanism of Action: Inhibits mycobacterial cell wall synthesis and interferes with
metabolism
Therapeutic Effect: Bacteriostatic or bactericidal effect against susceptibl\e mycobcteria
Dosage,Route,Frequency:
 Adult
PO  300mg/day (5 mg/kg) or 15 mg/kg (up to 900 mg) 2-3 times weekly
 Children
PO 10-20 mg/kg/day (up to 300 mg/day) or 20-40 mg/kg (up to 900 mg) 2-3
times weekly
Nursing Interventions Rationale
1) Instruct patient that he/she may take This drug may cause gastric irritation
medications with food or antacids
2) Advise patient to take medication as To ensure therapeutic effect. Doubling up the
directed. Take missed doses as soon as dose may have toxic effect
possible unless almost time for next dose; do
not double up on missed doses. Emphasize the
importance of continui.ng therapy even after
symptoms have subsided. Therapy may be
continued for 6 months to 2 years.
3) Advise patient to notify health care
professional promptly if the following These are signs and symptoms of hepatitis
happens:
 Jaundice
 Vomiting
 Anorexia
 Unusual tiredness
 Weakness
 Dark urine
4) Caution patient to avoid the use of alcohol This may increase the risk for hepatotoxicity
during the therapy
5) Advise patient to avoid taking tyramine-rich This may result in redness or itching of the
foods while taking the drug skin; hot feeling; rapid or pounding heartbeat;
sweating; chills; cold clammy feeling;
headache or lightheadedness

3) Generic Name: Pyrazinamide

Classification: Antituberculars
Mechanism of Action: Mechanism not known
Therapeutic Effect: Bacteriostatic action against susceptible mycobacteria
Dosage,Route,Frequency:
 Adult and Children
PO  15-30 mg/kg/day as a single dose. May also be given as 50-70 mg/kg 2-3
times weekly
Nursing Interventions Rationale
1) Advise patient to take medication as To ensure therapeutic effect. Doubling up the
directed and not to skip doses or double up on dose may have toxic effect
missed doses
2) Advise patient to use sunscreen and To prevent photosensitivity reaction
protective clothing
3) Evaluate hepatic function before and every To evaluate the need to take the drug. Patients
2-4 weeks during therapy with impaired liver function should receive
pyrazinamide therapy only if crucial to
treatment

4) Generic Name: Ethambutol

Classification: Antituberculars
Mechanism of Action: Inhibits the growth of mycobacteria
Therapeutic Effect: Tuberculostatic effect against susceptible oraganisms
Dosage,Route,Frequency:
  Adult and Children > 13 yr
PO  15-25 mg/kg/day (maximum 2.5 g/day) or 50 mg/kg (up to 2.5 g) twice
weekly or 25 -30 mg/kg (up to 2.5 g) 3 times weekly
Nursing Interventions Rationale
1) Advise patient to take medication with food To minimize gastric irritation
or milk
2) Advise patient to take medication as To ensure therapeutic effect. Doubling up the
directed and not to skip doses or double up on dose may have toxic effect
missed doses
3) Instruct patient to notify HCP if unexpected These are adverse reactions of the drug
weight gain or decreased urine output occurs
4) Perform opthalmoscopic examination prior This drug may cause ocular toxicity
to and at monthly intervals during therapy
5) Instruct patient to adhere to drug regimen To prevent drug resistance

5) Generic Name: Streptomycin

Classification: Aminoglycoside
Mechanism of Action: Binds to negatively charged sites on the bacteria’s outer cell
membrane, disrupting cell integrity. It also binds to bacterial ribosomal subunits and
inhibits protein synthesis
Therapeutic Effect: Bactericidal
Dosage,Route,Frequency:
 Adult
IM  15 mg/kg up to 1 g/day as single dose
 Children
IM  20-040 mg/kg/day up to 1 g/day
Nursing Interventions Rationale
1) Advise patient to report severe headache, These indicate damage to vestibular position of
nausea, vomiting, vertigo in upright position, 8th cranial nerve
difficulty in reading, unsteadiness, and positive
Romberg’s sign
2) Monitor I and O Urticaria or changes in I and O may indicate
signs of diminishing kidney function

GENERAL NURSING INTERVENTIONS

Nursing Interventions Rationale
1) Encourage patient to increase fluid To promote systemic hydration and this
intake serves as an effective expectorant
2) Teach patient about DBE To facilitate airway drainage
3) Educate the patient that TB is a To promote adherence to drug regimem
communicable disease and taking of
medication is the most effective means of
preventing transmission. Also, instruct
patient about the risk of drug resistance if
the medication regimen is not strictly and
continuously followed.
4) Instruct the patient to take the To avoid interference with medication
medication on an empty stomach or at absorption
least 1 hour before meals
5) Patients taking INH should avoid This may result in headache, flushing,
foods that contain tyramine and histamine hypotension, lightheadedness,
(tuna, aged cheese, red wine, soy sauce, palpitations, and diaphoresis
yeast extracts)

Patients should also avoid drinking This may reult in hepatoxic effects
alcohol
6) Instruct the patient not to take rifampin Rifampin can alter the metabollism of
concurrently with beta-blockers, oral these drugs making them less effective
anticoagulants (warfarin), digoxin,
quinidine, corticosteroids, oral
hypoglycemic agents, oral contraceptives,
theophylline, and verapamil (Calan,
Isoptin)
7) Inform the patient that he/she may Rifampin may discolor contact lenses
wear eyeglasses during the treatment Some drugs may have photosensitivity
effect
8) Liver enzymes, BUN, and serum To detect changes in liver and kidney
creatinine levels should be monitored function
9) Sputum culture results should be To evaluate the feffectiveness of the
monitored for AFB (acid-fast bacilli) treatment regimen and adherence to
therapy
10) Plan a meal that allows for small, To promote nutrition. Small and frequent
frequent meals meals because the patient may be too
tired to eat due to excessive coughing.
Liquid nutritional supplements may be To assist in meeting basic caloric
required requirements
11) Educate the patient about the This measures prevent the transmission
importance of hygiene measures, of tuberculosis infection
inclusing mouth care, covering the mouth
and nose when coughing and sneezing,
proper disposal of tissues, and hand
hygiene

References
Hinkle and Cheever (2014).Brunner and Suddarth’s Textbook of Medical-Surgical
Nursing 13th edition.Philadelphia:Lippimcott Williams & Wilkins.
http://www.who.int/mediacentre/factsheets/fs104/en/ retrieved on March 2017.
http://www.tbfacts.org/tb-tests/
In partial fullfillment of the

requirement in

RLE 104B

Submitted to:

Prof. Precy Oducayen

Prof. Julie C. Damaso
Prof. Marilyn Racca

Submitted by:

Angelic I. Mateo
Ivy A. Encinares
Angelique Joyce D. Vermudez

July 01, 2018