Pulmonary Tuberculosis

Tuberculosis (TB) is an infectious disease caused by Mycobacterium

tuberculosis, an aerobic acid-fast bacillus. Although it is most frequently a
pulmonary disease, more than 15% of patients experience extrapulmonary TB that
can infect the meninges, kidneys, bones, or other tissues. Pulmonary TB can range
from a small infection of bronchopneumonia to diffuse intense inflammation,
necrosis, pleural effusion, and extensive fibrosis. Although TB was thought to be
preventable and treatable, the number of cases increased during the late 1980s. In
1990, more than 25,000 cases were reported in the United States, which was a 10%
increase from the previous year. The increase was thought to be due to a high
infection rate in patients with the human immunodeficiency virus (HIV) and patients
who were exposed to others hospitalized with TB, as well as a new strain of the
disease that is resistant to traditional drugs such as isoniazid (INH) and rifampin.
Recent decreases are due to intensive public health efforts to prevent and control
the disease.

Primary Tuberculosis
Primary tuberculosis occurs in a person lacking previous contact with the
tubercle bacillus. It typically is initiated as a result of inhaling droplet nuclei that
contain the tubercle bacillus. Inhaled droplet nuclei pass down the bronchial tree
without settling on the epithelium and implant in a respiratory bronchiole or
alveolus beyond the mucociliary system. Soon after entering the lung, the bacilli are
surrounded and engulfed by macrophages. M. tuberculosis has no known
endotoxins or exotoxins; therefore, there is no early immunoglobulin response to
infection.
Secondary Tuberculosis
Secondary tuberculosis represents either reinfection from inhaled droplet
nuclei or reactivation of a previously healed primary lesion (see Fig. 30-3). It often
occurs in situations of impaired body defense mechanisms. The partial immunity
that follows primary tuberculosis affords protection against reinfection and to some

extent aids in localizing used for control testing are Candida, mumps virus, and
tetanus toxoid. Most healthy persons in the population have been exposed to these
antigens and will display a positive response to these control tests.
Classification of TB
Data from the history, physical examination, skin test, chest x-ray, and
microbiologic studies are used to classify TB into one of five classes. A classification
scheme provides public health officials with a systematic way to monitor
epidemiology and treatment of the disease (American Thoracic Society, 2000).
Class 0: no exposure; no infection
Class 1: exposure; no evidence of infection
Class 2: latent infection; no disease (eg, positive PPD reaction but no clinical
evidence of active TB)
Class 3: disease; clinically active
Class 4: disease; not clinically active
Class 5: suspected disease; diagnosis pending

Peripheral arterial occlusive disease (PAOD) results either from atherosclerotic or inflammatory
processes causing lumen narrowing (stenosis), or from thrombus formation (usually associated
with underlying atherosclerotic disease). When these conditions arise, there is an increase in
vessel resistance that can lead to a reduction in distal perfusion pressure and blood flow. The
following discussion assumes chronic atherosclerotic conditions in the human lower limb that
result in stenotic lesions. The hemodynamics and underlying mechanisms of PAOD in the
human limb are very similar to what is found in coronary artery disease.
A common site for PAOD is in the leg (see figure at right). The circulation to the leg is derived
from the femoral artery that is a continuation of the external iliac artery. A major branch from the
femoral artery is the deep femoral artery. Distal to the deep femoral branch, the femoral artery
(sometimes referred to as the superficial femoral artery at this point) continues down the leg and
becomes the popliteal artery just above the knee. Two major arteries at the termination of the
popliteal artery are the anterior and posterior tibial arteries, which supply blood flow to the lower
leg and foot.

Signs and symptoms:

PTB

Cough

Unintentional weight loss

Fatigue

Fever

Night sweats

Chills

Loss of appetite

PVD:
Pain (on legs)
Muscle weakness
Fatigue
Numbness
Coldness
Leg ulcers

Predisposing factors:

Precipitating factors:

Lack of medical care

Substance abuse

Living or working in a crowded area

Close contact with someone with active TB

HIV/AIDS

Diabetes

End-stage kidney disease

Cancer treatment (chemotherapy)

Drugs to prevent rejection of transplanted organs

Some drugs used to treat rheumatoid

65 years old

arthritis, Crohns disease and psoriasis

Malnutrition

Advanced age

Increased susceptibility to infections

Inhalation of mycobacterium bacilli

Bacteria transmitted through airway

Deposited to alveoli and begin to multiply

Inflammatory reaction initiated

Phagocytes engulf bacteria

TB-specific lymphocytes lyse bacilli

Accumulation of exudates in alveoli

productive cough

Macrophages surround new tissue masses

of live and dead bacilli

protective wall formed around granulomas

hemoptysisbacteria and macrophages become necrotic

becomes calcified and form collagenous scar

chest pain

bacteria become dormant

PULMONARY TUBERCULOSIS

Loss of

appetite
Nausea
Vomiting

Weight loss

Reduced distal perfusion pressure

Decreased flow
Predisposing Factors:
Precipitating

Sex
65 y.o.
Age
Male
Smoking
Smokes 1-3 packs/day
Diabetes
Hypertension
Dyslipidemia
Atherosclerosis

Stenosis formation

Decreased distal peripheral perfusion pressure

Increased resistance to flow

Reduced blood flow to distal parts

Increance oxygen demand

Hypoxia

Fatigue

Ischemia
ischemic area

weakness of the
Pain at rest

PERIPHERAL VASCULAR DISEASE

Stenotic lesions

Reduced oxygen supply

Inflammatory process unable to take place

Ulcers

Damage to blood vessels, nerves and underlying tendons

Death of cell tissue

Necrosis

Pulmonary Tuberculosis
Medical Management

Complete history, physical examination, tuberculin skin test, chest x-ray,

acid-fast bacillus smear, and sputum culture are obtained

chemotherapeutic agents(antituberculosis agents) for 6 to 12 months
Recommended treatment guidelines for newly diagnosed cases of pulmonary
TB (CDC, 2000) consist of a multiple-medication regimen of INH, rifampin,
pyrazinamide, and either streptomycin
or ethambutol.

Nursing Management

Promoting airway clearance:

1. Increase fluid intake to promote systemic hydration and serves as an
effective expectorant.
2. Correct positioning to facilitate airway drainage.
3. Deep breathing and coughing exercises.
Advocating adherence to therapeutic regimen:
1. Assesses the patients living arrangements, perceptions and
understanding of TB and its treatment, and readiness to learn.
2. Encourage patient to comply with treatments and medications.
3. Instruct patient about important hygiene measures, including mouth care,
covering the mouth and nose when coughing and sneezing, proper

disposal of tissues, and hand hygiene.

4. Explain to patient and family possible side effects of mediacations.
Promoting Activity and Adequate Nutrition
1. Plan a progressive activity schedule that focuses on increasing activity
tolerance and muscle strength.
2. Nutritional plan that allows for small, frequent meals may be required.
Liquid nutritional supplements may assist in meeting basic caloric

requirements.
Monitoring and Managing Possible Complications
1. Since malnutrition is one of the possible complications, the nurse must
collaborate with the dietitian, physician, social worker, family, and patient
to identify strategies to ensure an adequate nutritional intake and
availability of nutritious food.
2. Assess side effects of medications.
3. Monitor vital signs and observe for spikes in temperature or changes in
the clinical status.
4. Instruct the patient the risk of multi-drug resistance if the medication
regimen is not strictly and continuously followed.