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Presentation outline
INTRODUCTION
 DEFINTION
 PATHOPATHOLOGY
 RISK FACTORS
 CLINICAL FEATURES
 DIAGNOSIS
 MANAGEMENT
 COMPLICATION

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INTRODUCTION
 COPD, a common preventable and treatable disease, is
characterized by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic
inflammatory response in the airways and the lung to noxious
particles or gases.
 COPD is also known as chronic obstructive lung disease
(COLD), chronic obstructive airway disease (COAD), chronic
airflow limitation (CAL) and chronic obstructive respiratory
disease (CORD)
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Cont----------• This leads to a limitation of the flow of air to
and from the lungs causing shortness of breath.
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In COPD, less air flows in and out of the airways because of one
or more of the following:
⚫ The airways and air sacs lose their elastic
quality.
⚫ The walls between many of the air sacs are
destroyed.
⚫ The walls of the airways become thick and
inflamed.
⚫ The airways make more mucus than usual,
which tends to clog them.
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Incidence
⚫It is the 4th leading cause of mortality and 12th
leading cause of disability in the united states.
⚫In 2023 COPD is the 3rd leading cause of
death.
⚫In Ethiopian study that the prevalence of
COPD is high. Factors such as old age,
cigarette smoking, exposure to biomass
smoke and poor kitchen ventilation plays
a role in the development of COPD.
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RISK FACTORS FOR COPD
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Cont-------- Smoking. Smoking is primary risk factors for
COPD. The numerous irritants found in cigarette
smoke stimulate excess mucus production and
coughing, destroy ciliary function and lead to
inflammation and damage of bronchiolar and
alveolar walls.
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Cont--------• Air pollution high levels of urban air
pollution are harmful to persons with existing
lung disease. However, the effect of outdoor
air pollution as a risk factor for COPD.
Another risk factor for COPD development is
fossil fuels that used for indoor heating and
cooking.
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Cont------• Occupational exposures- exposure to
workplace dusts found in coal mining, gold
mining, and the cotton textile industry and
chemicals such as cadmium, and fumes from
welding have been implicated in the
development of airflow obstruction. Exposure
of these irritants causes the airway to be hyper
responsive.
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Cont----• Infection :infections is risk factor for
developing COPD. Severe recurring
respiratory tract infection in childhood have
been associated with reduced lung function
and increased respiratory symptoms in
adulthood. Recurring infections impair normal
defense mechanisms, making bronchioles and
alveoli more susceptible to injury.
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Cont----• Genetics-Alpha 1-antitrypsin deficiency is a
genetic condition that is responsible for about
2% of cases of COPD. In this condition, the
body does not make enough of a protein, alpha
1-antitrypsin. Alpha 1- antitrypsin protects the
lungs from damage caused by protease
enzymes, such as elastase and trypsin, that can
be released as a result of an inflammatory
response to tobacco smoke
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Pathophysiology
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Cont------• COPD is characterized by airflow limitation
that is poorly reversible. chronic exposure to
cigarette smoking is the number one cause of
the disease, but repeated exposure to
secondhand smoke,
• air pollution and occupational exposure (to
coal, cotton, grain) are also important risk
factors.
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Cont.-----• Smoking and other airway irritants cause
neutrophils, T-lymphocytes, and other
inflammatory cells to accumulate in the
airways. Once activated, they trigger an
inflammatory response in which an influx of
molecules, known as inflammatory mediators,
navigate to the site in an attempt to destroy
and remove inhaled foreign debris.
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Cont.-----• Under normal circumstances, the inflammatory
response is useful and leads to healing. In fact,
without it, the body would never recover from
injury. In COPD, repeated exposure to airway
irritants perpetuates an ongoing inflammatory
response that never seems to shut itself off.
Over time, this process causes structural and
physiological lung changes that get
progressively worse.
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Cont.-----• As inflammation continues, the airways
constrict, becoming excessively narrow and
swollen. This leads to excess mucus
production and poorly functioning cilia, a
combination that makes airway clearance
especially difficult. When people with COPD
can not clear their secretions, they develop the
hallmark symptoms of COPD, including a
chronic, productive cough, wheezing and
dyspnea.
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Cont.-----• Finally, the build-up of mucus attracts a host
of bacteria that thrive and multiply in the
warm, moist environment of the airway and
lungs.
• The end result is further inflammation, the
formation of diverticula in the bronchial tree,
and bacterial lung infection, a common cause
of COPD exacerbation.
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CLINICAL FEATURES
⚫Chronic cough
⚫Sputum production(yellow or green)
⚫Wheezing
⚫Chest tightness
⚫Dyspnoea on exertion
⚫Wt.loss
⚫Respiratory insufficiency
⚫Respiratory infections
⚫Barrel chest- chronic hyperinflation leads to
loss of lung elasticity.
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Conet----• Chronic obstructive pulmonary disease
(COPD) refers to chronic bronchitis and
emphysema, a pair of two commonly coexisting diseases of the lungs in which the
airways become narrowed.
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Bronchitis
⚫ Bronchitis results from inflammation of bronchi
leading to increased musus production, cough and
eventual scaring of the bronchial lining.
⚫ acute (short term) Infections or lung irritants cause
acute bronchitis.
⚫ chronic is an ongoing, serious condition. It occurs
if the lining of the bronchial tubes is constantly
irritated and inflamed, causing a long-term cough
with mucus
⚫ It is defined as the presence of cough and sputum
production for at least 3 months.
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Cont----Chronic bronchitis is characterized by the
following :
⚫A increased in size and number of
submucus glands in the large bronchi,
which increase mucus production.
⚫An increased number of goblet cells which also
secrete mucus.
⚫Impaired cillary function which reduce
mucus clearance.
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Signs and symptoms-Acute
⚫sore throat,
⚫fatigue (tiredness),
⚫fever, body aches,
⚫stuffy or runny nose,
⚫vomiting, and
⚫Diarrhea
⚫persistent cough
⚫cough may produce clear mucus
⚫shortness of breath
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Chronic symptoms
⚫coughing,
⚫ wheezing, and
⚫chest discomfort.
⚫The coughing may produce large amounts of
mucus. This type of cough often is called a
smoker's cough.
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EMPHYSEMA
• Emphysema is defined as enlargement of the
air spaces distal to the terminal bronchioles,
with destruction of their walls of the alveoli.
• As the alveoli are destroyed the alveolar
surface area in contact with the capillaries
decreases.
• Causing dead spaces (no gas exchange
takes place) Leads to hypoxia.
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In later stages:
CO2 elimination is disturbed and increase in CO2
tension in arterial blood causing respiratory acidosis
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There are three types of emphysema
1.
2.
3.
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Centriacinar
Panacinar
Paraseptal
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1. Centriacinar(centrilobular) emphysema the most
common type produce destruction in bronchioles
usually in the upper lung region. Inflammation
begins in the bronchioles and spread peripherally but
usually the alveolar sac remains intact. This form of
emphysema occurs most often in smokers.
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2.Panicar emphysema destroys the entire alveolus and
most commonly involves the lower portion of the lung.
This form of disease is generally observed in individuals
with ATT deficiency.
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3.Paraseptal or distal acinar emphysema primarily
involves the distal airway structures alveolar ducts
and alveolar sacs. The process is localized around the
septa of the lung or pleura. It is believed to be the
likely cause of spontaneous pneumothorax
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DIAGNOSIS
 Blood Test
 Chest X-ray or CT scan
 Sputum Examination
 ECG
 Pulmonary Function Test
 Spirometry
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Blood Test
• Blood tests can help determine if symptoms are
being caused by an infection.
• An arterial blood gas test will measure the
amount of oxygen in blood. This is one
indication of how well lungs are working. This
can help doctor determine how severe COPD
is and whether need oxygen therapy.
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Chest X-ray or CT scan
. A CT scan is a type of X-ray that creates a more
detailed image than a standard X-ray. Whichever type
doctor chooses, an X-ray will give a picture of the
structures inside chest. These include your heart, lungs,
and blood vessels. Your doctor will be able to see if
client has evidence of COPD. If symptoms are being
caused by another condition such as heart failure, the
doctor will be able identify that as well
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Sputum Examination
 Doctor may order a sputum examination, especially
if the client has a productive cough. Sputum is the
mucus the client cough up.
 Analyzing sputum can help identify the cause of
breathing difficulties and may rule out some lung
cancers. If there is a bacterial infection, it can be
identified and treated.
ECG
 The doctor might request an ECG to determine if
your shortness of breath is being caused by a heart
condition.
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Pulmonary Function Test
⚫ pulmonary function tests (PFTs) measure how well
the lungs are moving air in and out. They also
measure how well the lungs are moving oxygen to the
blood.
⚫ Spirometry (meaning the measuring of breath) is the
most common of the pulmonary function tests (PFTs).
It measures lung function, specifically the amount
(volume) and/or speed (flow) of air that can be
inhaled and exhaled.
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MANAGEMENT
⚫MEDICAL MANAGEMENT
⚫SURGICAL MANAGEMENT
⚫NURSING MANAGEMENT
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MEDICAL MANAGEMENT
The treatment goal for the client with COPD are:
 To improve ventilation
 To facilitate the removal of bronchial secretions
 To promote health maintenance
 To reduce complications, and
 To slow progression of the disease
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Smoking cessation
Cessation of cigarette smoking is single most
effective and cost effective intervention to
reduce the risk of developing COPD and stop
the progression of the disease. After
discontinuation of smoking, the accelerated
decline in pulmonary function slows and
pulmonary function usually improves.
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Drug therapy
 Reduce symptoms
 Increase the capacity of exercise,
 Improve overall health and
 Reduce the severity of exacerbations.
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Bronchiodilator drug therapy
are agents that widen the air passages by relaxing the
bronchial smooth muscle and improve the ventilation
of lungs. They are usually administered via inhalation
route but in rare occasions may be given orally or
administered intravenously. Regular treatment with
long acting bronchiodilators is more effective and
convenient than treatment with short acting forms.
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Cont--------The principal bronchiodilator treatment are Beta2
agonists, anticholinergics, and methylxanthines
used singly or combination.
The choice of bronchioldilators depends on
availability and patient’s response.
Beta2 agonists are sympathomimetic drugs that acts on
the beta-adrenoceptors in the smooth muscles of the
airway and cause bronchioldilation. These drugs may
also enhance mucus clearance and improve the
endurance of respiratory muscles.
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Cont--------⚫ Short acting Beta2 agonists(e.g., albuterol)have minimal
adverse effects with rapid onset of action, a peak effect in 60
to 90 minutes and duration of 4 to 6 hour.
⚫ Side effects that may develop with the use of these drugs
are tachycardia, tremor, nervousness, and nausea.
⚫ Anticholinergic agents offer greater bronchiodilator effect
and fewer side effect than short acting inhaled beta2 agonists.
⚫ These drugs work by blocking the cholinergic receptors
located in the larger airways, resulting in bronchiodilation.
Ipratropium(atrovent) is the most commonly used drug in this
category.
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Cont--------Three major classes of bronchodilators:
β2 - agonists:
Short acting: salbutamol & terbutaline
Long acting :Salmeterol & formoterol
Anticholinergic agents:
Ipratropium,tiotropium
Theophylline (a weak bronchodilator, which may
have some anti-inflammatory properties)
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Cont--------polysaccharide vaccine is recommended for COPD
patients 65 years and older and for COPD patients
younger than age 65 with an FEV1 < 40% predicted.
The use of antibiotics, other than for treating infectious
exacerbations of COPD and other bacterial infections, is
currently not indicated.
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Oxygen therapy
 O2 therapy is frequently used in the treatment of
COPD another problem associated with
hypoxemia. Long term o2 therapy improves
survival, exercise capacity, cognitive performance
and sleep in hypoxemic patients.O2 is colorless,
odorless testless gas that constitutes 20.95% of the
atmosphere. O2raises the partial pressure of
oxygen(PO2) in inspired air.
Indications for use: goals for 02 therapy are
⚫ To reduce the work of breathing,
⚫ To maintain the PaO2
⚫ To reduce the workload of heart
⚫ To keep the SaO2 more than 90% during rest
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Cont----Oxygen is usually administered to treat
hypoxemia caused by
⚫Respiratory disorders such as COPD pulmonary
hypertension pneumonia and pulmonary emboli
⚫Cardiovascular disorders such as myocardial
infraction, angina pectoris and cardiogenic shock
⚫Central nervous system disorders such as overdose
of opiods
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SURGICAL MANAGEMENT
 bullectomy
Bullae are enlarged airspaces that do not contribute to
ventillation but occupy space in the thorax,these
areas may be surgically excised
 lung volume reduction surgery
It involves the removal of a portion of the diseased
lung parenchyma.this allows the functional tissue
to expand.
 lung transplantation
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Nursing management
•
•
•
•
•
Nursing diagnosis
Impaired gas exchange related to decreased ventilation
Objectives
Improve ventilation
Intervention
a. Monitor lung sounds every 4 to 8 hours.
b. Perform chest physiotherapy
c. Advice the client to drink at least 8 to 10 glasses of fluid
per day unless contraindicated
d. Teach the client in coughing technique
e. Asses the condition of oral mucus membrane and
perform oral care
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Nursing diagnosis
• Disturbed sleep pattern related to dyspnea
• Objectives
• Getting adequate rest
• Intervention
⚫ Promote relaxation by providing a darkened, quiet
environment, ensure adequate room ventilation.
⚫ Avoid use of sleeping pills
⚫ Schedule care activities to allow periods of
uninterrupted sleep.
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Cont--------Nursing diagnosis
Activity intolerance related to inadequate
oxygenation
Objective
Improve to perform daily activity
Intervention
⚫ Monitor the severity of dyspnea
⚫ Stop or slow any activity that leads to change in
respiratory rate
⚫ Advice the client to avoid conditions that
increase oxygen demand
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Cont-----Nursing diagnosis
Anxiety related to acute breathing difficulties and fear of
suffocation
Objectives
Relieve fear of dying
Intervention
⚫ Provide a quiet, calm environment.
⚫ During acute episodes, open doors and curtains and limit the
number of people in the room.
⚫ Encourage the use of breathing retraining and relaxation
technique
⚫ Give sedative and tranquilizers with extreme caution.
⚫ Nonpharmacological methods of anxiety reduction are more
useful
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Cont----Nursing diagnosis
Ineffective airway clearance related to excessive secretions and
ineffective coughing
Objective
Effective airway clearance
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Complications
⚫ More frequent lung infections, such as
pneumonia.
⚫ An increased risk of thinning bones
(osteoporosis), especially if you use oral
corticosteroids.
⚫ Problems with weight. If chronic bronchitis is the
main part of your COPD.
⚫ Heart failure affecting the right side of the heart
(cor pulmonale).
⚫ A collapsed lung (pneumothorax).
⚫ Sleep problems.
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COPD Comorbidities
COPD patients are at increased risk
for: Cardiovascular diseases
Osteoporosis
Respiratoryinfections
Anxiety and
Depression
Diabetes
Lung cancer
Bronchiectasis
These comorbid conditions may influence mortality and
hospitalizations and should be looked for routinely, and treated
appropriately.
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Differential Diagnosis of COPD
Chronic Asthma
Bronchiectasis
Bronchial carcinma
Heart failure
Pulmonary TB
And others
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Differentiating COPD and Asthma
Asthma
COPD
Early in life (often childhood)
Mild-life
triggers
allergens
Cigarette smoke
occupational pollutants
symptoms
variable
Slowly progressive
Airflow
limitation
Largely reversible
Partially reversible
Clinical features
Episodic wheeze chest,
tightness cough ,dyspnea
Chronic dyspnea, cough,
sputum,wheeze
Inflammatory
cells
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Primarily eosinophils
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Primarily neutrophils
onset
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INTRODUCTION
• Chronic (sometimes acute or sub acute),
debilitating and notifiable disease
characterized by formation of tubercles in
lungs and other tissues of the body
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Pulmonary Tuberculosis (PTB)
 Tuberculosis (TB) is an infectious disease that primarily
affects the lung parenchyma in which case it is called
pulmonary TB.
 In addition to the lungs, any part of the body can be
affected with this bacterium and in this case it is called
extra pulmonary TB.
 TB affects individuals of all ages and both sexes, and
estimated to infect 1/3 of world population leaving
increased pool of vulnerability to develop active.
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Infectious agent
1. M. tuberculosis :- human tubercle bacilli (commonest cause)
[90%]
2. M. bovis:- causes cattle ,unpasteurization milk and man
infection[5%].
3. M. avium:- causes infection in birds and man
4. M. africanum is not widespread, but in parts of Africa it is a
significant cause of tuberculosis
5. M. Canetti is rare and seems to be limited to Africa, although a
few cases have been seen in African emigrants.
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M. microti is mostly seen Byinsaniimmunodeficient people
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Epidemiology of TB
 TB affects an estimated 10 million people per year (range 8.9–
11.0 million) and is one of the world’s leading infectious disease
killers. Due to malnutrition, immunity, overcrowded, susceptible
 Of the estimated 10 million, approximately 70% are diagnosed
and treated and also reported to the WHO, resulting in 7.1 million
TB notifications by National TB Programme,
 Of the 7.1 million persons notified in 2019, 5.9 million (84%)
had PTB (WHO consolidated guidelines on TB 2022)
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TB situations in Ethiopia
 TB remains a major public health problem worldwide and leading
cause of morbidity and mortality.
 Currently, 1.7 billion (26%) of the world’s population are
considered to be infected with MTB.
 In Ethiopia, TB is a major public health problem.and
 in 2023 E.c list of 10 top diseases placed fifth (5)
 The country is still among the 22 high TB burden countries with
high number of missed and infectious TB cases in the community.
 TB is among the top ten causes of admission and deaths in adults.
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Epidemiology of TB…
It is also estimated that Ethiopia had 191,000 new TB
cases in 2015.
This number ranks Ethiopia 10th globally and 4th in
Africa, after Nigeria, South Africa and the DR Congo.
Ethiopia is also one of the 27 countries with a high
burden of multidrug-resistant .(MDR)TB A study
conducted in Addis Ababa, Ethiopia showed that the
prevalence of both PTB and EPTB was 46.0% (Eshetu
Temesgen, etl, Addis Ababa, 2021)
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Epidemiology of TB…
 In Ethiopia, TB case detection is below the WHO target.
 In 2019, 29.3% of cases were not notified to the national
TB program
 The prevalence of pulmonary TB cases among people who
sought health care with cough of any duration was 16.7%,
of which 95.5% PTB cases were diagnosed at OPDs.
 Of 16.7% of TB cases, 60% was confirmed by sputum and
40%was confirmedby CXR, history & clinical.
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CONT…
 The prevalence of confirmed PTB among routine out
patients was high, and this included those with a low
duration of cough who can serve as a source of
infection.
 Screening all patients at outpatient departments who
passively report any cough irrespective of duration is
important to increase TB case finding and reduce TB
transmission and mortality (Hussen M, etl, Ethiopia,
2020)
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CONT…

TB related mortality is high lighted in the top ten reported
causes of death among hospital admissions, with annual
estimated death rate of 26 per 100,000 populations in 2015.
 TB incidence 42% of decline from annual 369 cases per
100,000 populations to 177 per 100,000 populations in 2016
 Ethiopia remains to be among the 30 countries reported with
high burden of TB, TB/HIV and DR-TB for 2015 to 2020.
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CONT…
 In 2016, estimated 35% of incident TB cases were
missed
 TB remains to be the leading causes of death of
people with HIV, accounting for around 40% of
AIDS-related deaths.
 Both diseases together form a lethal combination,
each speeding the other's progress.
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Cont---------- In Ethiopia, 82% of notified TB patients in 2016 knew their
HIV status while 82% of reported HIV-positive TB patients
have accessed antiretroviral therapy.
• HIV infection and TB disease on same year leaving people at
increased risk of suffering & mortality
MDG achieved
 HIV prevalence in incident TB cases (TB/HIV co-infection rate)
is about 11%, Global average 13%, African average 34%
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Cont------ Ethiopia adopted the DOTS strategy since 1997 after
successful pilot program with the development of the
first combined TB and Leprosy Prevention and Control
Program manual.
 TB/HIV collaborative activities were piloted in 2004 and
subsequently scaled up national (Ethiopia National
guideline for TB Leprosy and TB 6th edition Aug-2018)
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TB Control strategy
 Globally different control strategies were implemented for the
past two decades to reduce morbidity and mortality due to TB
all over the world. These strategies were, DOTS (directly
observed treatment, short-course) strategy of 1995.
 The stop TB Strategy of 2006 that aided to reduce all forms
of TB including HIV-associated and drug-resistant TB
 These strategies got remarkable achievement in that 37 million
lives were saved between 2000 and 2013/15
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TB Control strategy…
Recently, WHO developed the end TB strategy with
an overall goal of a 90% reduction in TB incidence
and a 95% reduction in TB deaths from 2015 to 2035
by integrated patient-centered care and prevention,
bold policies and supportive systems, intensified
research and innovation (Eshetu Temesgen, etl,
Addis Ababa, 2021)
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Ethiopia TB Roadmap Overview,2022-2026
 Among the top 30 high TB burden countries, Ethiopia
ranked 12th; and among the high multidrug-resistant TB
(MDR-TB) burden countries, Ethiopia ranked 24th .
 While some gains have been made in decreasing TB
incidence, from 421 (in 2000) to 132 (in 2020) per 100,000, of
incidence and mortality from drug-susceptible TB remain
high, while treatment coverage remains low.
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By Prioritizing the following interventions
1. Scaling-up the use of rapid diagnostics for routine screening
2. Engaging all care providers in TB diagnosis and care;
3. Prioritizing reaching vulnerable populations
4. Decentralization of TB care and treatment;
5. Mitigating the catastrophic cost of TB care on patients and HHS
6. Increasing contact screening coverage and preventive treatment
7. Mitigating TB-related stigma in the community and healthcare
8. Proactively finding ways to manage other respiratory impacts
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Transmission of TB
 TB spreads from person to person by airborne transmission.
 An infected person releases droplet nuclei (usually particles 1
to 5 mcm in diameter) through talking, coughing, sneezing,
laughing, or singing.
 Larger droplets settle; smaller droplets remain suspended in
the air and are inhaled by a susceptible person.
 ingestion of unpasteurised infected milk
• NB: TB becomes non-infectious 2-4 weeks after starting
treatment. It is not highly infectious and cannot be spread by
hands, books, glasses, dishes or formites
• Incubation period : 2-10 weeks. May be latent for several
decades
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Lists risk factors for TB
Close contact with some one who has active TB
Immuno compromised status e.g. pregnant mothers,
HIV/AIDS, Immuno suppressant drugs, chronic illness, DM
Substance abuse (IV/injection drug users and alcoholics).
Any person without adequate health care
Pre existing medical conditions or special treatment
Immigration from or recent travel to countries with a high
prevalence of TB.
Institutionalization
Living in overcrowded, substandard housing.
Being a health care worker performing high-risk activities
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Pathophysiology
 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.
 The body’s immune system responds by initiating an
inflammatory reaction
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Cont----- Phagocytes (neutrophils and macrophages) engulf many of
the bacteria, and TB-specific lymphocytes 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.
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Cont.---- 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 &
activation of dormant bacteria.
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Cont.---- 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.
 THIS CAUSES the infected lung to become more
inflamed, resulting in the further development of
bronchopneumonia and TB formation.
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Evolution of TB infection and disease
1. Latent TB infection: Individuals with latent TB
infection do not have symptoms as there is no tissue
destruction by the bacilli and are not infectious.
In immuno competent individuals, only 5-10% of
infected persons develop active disease in their life
time.
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CONT…
2. Active TB disease : may arise from progression of the
primary lesion after infection (Primary TB), or from
endogenous reactivation of latent foci, which remained
dormant.
 The progression from LTBI to Active TB disease may
occur at any time, from soon to many years later.
 Post primary/secondary TB usually affects the lungs
(Pulmonary TB) and
 If it disseminated, to all organs can be affected
(MiliaryTB)
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CONT….
3. Prognosis of TB: In the great majority (90-95%) of
persons infected with MTB, the immune system either
kills the bacilli or perhaps more often, keeps them
suppressed (silent focus) resulting a latent TB
infection
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Registration group for TB patient
New TB: patients that have never been treated for TB or have
taken anti-TB drugs for less than one month.
Relapse: patients who were declared cured or treatment
completed at the end of their most recent treatment course, and is
now diagnosed with a recurrent episode of TB.
Treatment after failure: refers to patients who were declared
treatment failure in their most recent course of treatment as
per national protocol.
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cont…
Treatment after loss to follow-up: refers to patients
who were declared lost to follow-up at the end of their
most recent course of TB treatment and is now decided
to be treated with full course of TB treatment.
Transfer in: A patient who is transferred to continue
treatment at a given reporting unit after starting
treatment in another reporting unit.
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Clinical features
 The clinical features of TB depend on the specific
organ affected.
 The clinical features can be grouped:
1. General (non-specific) and
2. Organ specific
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Clinical features….
Tuberculosis has two major clinical forms
Pulmonary (80%) of the total TB cases.

Primarily occurs during child hold & secondarily 15-45
years or later.
Extra pulmonary (20%) affects all parts of the body.
Most common sites are lymph nodes, pleura, GUT,

bone and joints, meninges & peritoneum.
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General symptoms of TB







Weight loss
Fever
Night sweats
Loss of appetite
Fatigue
Malaise
Malnourished and chronically sick appearance
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Organ specific
Pulmonary tuberculosis
 Cough that lasts for more than 2weeks with or without
sputum production
 Chest pain
 Hemoptysis
 Shortness of breath
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Cont------Tuberculosis lymphadenitis
 Slowly growing painless lymph node enlargement
 Initially firm and discrete, later become matted and
fluctuant
 Formation of abscesses and discharging sinuses,
which heal with scarring
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Cont------Tuberculous pleurisy
 Pleuritic chest pain (pain while breathing /coughing
/sneezing)
 Intermittent cough
 Shortness of breath
 Signs of pleural effusion (dullness, decreased/absent
air entry and decreased tactile fremitus)
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Cont------TB of bones and or joints

Localized pain and or swelling +/-discharge ,stiffness of joints
 Spine(TB spondylitis):localized swelling over the back ,back
pain paralysis (weakness of the lower extremities)
Abdominal TB
 Chronic non- specific abdominal pain with diarrhea or constipation

Fluid in the abdominal cavity(ascites).

Mass(inflammatory mass) in the abdomen
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Cont----------Tuberculous meningitis
 Head ache, fever, vomiting: insidious onset
 Neck stiffness, impaired level of consciousness.
Tuberculous pericarditis
 Chest pain (pleuritic)
 Shortness of breath
 Pericardial friction rub or distant t heart sound
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Tuberculosis in children
• has non specific features e.g. weight loss
fever, diarrhea, enlarged glands, fits, chronic
cough/wheeze which does not respond to
antibiotics
• TB is suspected in children with a history of
contact with a sputum positive patient
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Diagnosis of Pulmonary Tuberculosis in
Adult and Adolescents
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0
Investigations and diagnosis
The diagnosis of TB requires the following
 Clinical suspicion,
 Physical examinations and
 Microbiologic identification of the bacilli.
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Cont-------Sputum direct microscopy: Acid Fast Bacilli(AFB)
staining
 Three sputum specimens(Spot early morning-spot),
need to be collected and examined in two consecutive
days
 Result must be available on the second day.
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Cont--------Ꞝ Gene Xpert
 A fully automated DNA/molecular diagnostic test to
detect TB and Rifampicin resistance simultaneously.
 It is recommended as the initial diagnostic test for all
persons being evaluated for TB
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Cont--------Ꞝ Sputum culture and drug susceptibility
 Culture is the gold standard
 It takes weeks to get the results.

If sputum AFB and/or Gene Xpert are negative and there
is a strong suspicion, sputum culture can be send to a
referral laboratory.
 However, treatment for an alternative diagnosis or
“clinical TB”should not be delayed
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Cont-------Ꞝ Tuberculin Skin Test
 The Mantoux method is used to determine whether a person
has been infected with the TB bacillus
 Is used widely in screening for latent MTB infection.
 The Mantoux method is a standardized,intracutaneous
injection procedure.
 Purified protein derivative (PPD) 0.1 ml is injected into the ID
layer of the inner aspect of the forearm, approximately 4
inches below the elbow.
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Tuberculin Skin Test…
• The test result is read 48 to 72 hours after injection.
• Tests read after 72 hours tend to underestimate the
true size of induration (raised hard area or swelling).
• A delayed localized reaction indicates that the person
is sensitive to tuberculin
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Interpretations
 The size of the induration determines the significance of the
rxn.
 A reaction of 0 to 4 mm is considered not significant
 A reaction of 5 mm or greater may be significant in people
who are considered to be at risk.
 An induration of 10 mm or greater is usually considered
significant in people or positive
 In general, the more intense the reaction, the greater
the likelihood of an active infection.
 A negative tuberculin skin test doesn’t exclude TB, so its no
help in deciding that some one does not have TB.
(2018.14edi.Brunner & Suddarth’s Textbook of.pdf)
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cont-----




The criterion for a significant or 'positive' tuberculin test
depends on whether a child has previously had BCG
vaccination or not.
This is because a reaction to tuberculin is usual after a
previous BCG, for several years
A significant reaction indicates past exposure to M.
tuberculosis or vaccination with BCG.
The BCG vaccine is given to produce a greater resistance
to development of TB (60%-80% protect)
A positive tuberculin test is only one piece of evidence in
favor of the diagnosis of TB.
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Investigations and diagnosis…
Ꞝ Imaging:
 Chest X-ray:- patients who cannot produce sputum or
who have negative Xpert results. But CXR is nonspecific for TB
 Depending on the suspected extra pulmonary sites
other imaging modalities may be needed.
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Cont------Ꞝ Other investigation: HIV test, CBC, ESR, CSF analysis
 Body fluid analysis and identification of pathogen
 Tissue biopsy and histopathology
 Fine needle aspiration and histopathology
examination: enlarged lymph nodes
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Treatment of drug susceptible TB
Objectives
 Cure
 Prevent death from active TB or its late complications
 Restore quality of life and productivity
 Decrease transmission
 Prevent relapse
 Prevent the development and transmission of medicine
resistance
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Essential properties of TB treatment
In order to achieve the designed aim of treatment, an
anti-TB treatment regimen should be administered:
 In appropriate combination of drugs
 In the correct dosage
 Regularly taken by the patient, and
 For a sufficient period of time
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Non pharmacologic
 Counseling: adherence, the nature of treatment,
contact screening
 Good nutrition
 Adequate rest
 Admission for severely ill patients
E.g. Tb meningitis, pericarditis
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Pharmacologic
Standardized combination treatment:
All patients in a defined group receive the same
treatment regimen.
A combination of 4 or more anti-TB medicines.
Directly observed treatment (DOT)
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First line anti-TB Medicines
The first line anti-TB treatment available in Ethiopia are:
1. Rifampicin(R):the most bactericidal and potent sterilizing
agent
2. Isoniazid(H):highly bactericidal especially in the first few
days
3. Pyrazinamide (Z):only active in acidic environment and
bacilli inside macrophages
4. Ethambutol(E):bacteriostatic and effective to prevent drug
resistance when administered with other potent drugs
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Phases of chemotherapy
TB treatment is administered in two phases:
1. Intensive (initial) phase: aims to reduce the patient noninfectious by rapidly reducing the bacillary load in the
sputum and brings clinical improvement in most patients
receiving effective treatment.
2. Continuation phase: aims to sterilize the remaining semidormant bacilli and is important to ensure cure/completion of
treatment and prevent relapse after completion of Rx.
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A. Standardized first line treatment regimen for new
drug Susceptible or presumed to be drug susceptible TB
1.New pulmonary TB patients presumed or known to have
drug- susceptible TB
2. New extra pulmonary patients
 Standardized regimen: 6 months total (2months intensive and
4months continuation phase) : 2RHZE/4RH
 Intensive phase: 2 months Rifampicin, Isoniazid,
Pyrazinamide & Ethambutol (2RHZE)
 Continuation: 4months Rifampicin and Isoniazid (4RH)
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First line TB treatment adult dosing chart using
patient’s body weight
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B. Previously treated TB patients presumed or known to have
drug-susceptible TB
 In all previously treated TB patients who require retreatment, specimen for rapid molecular-based drug
susceptibility testing for first line TB drugs
 While awaiting the result, the standard first line
treatment regimen is recommended:2(RHZE)/4(RH)
 Re- treatment regimen” with addition of streptomycin
is not recommended.
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C. Patients who presented with active TB after known contact
with patient documented to have drug-resistant TB
 Sample should be sent for rapid drug susceptibility Test
(DST)
 Treatment should be decided based on rapid DST result.
 While awaiting DST result, the patient may be initiated
treatment with the regimen based on the DST of the
presumed source case.
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D. Extended continuation phase
 EPTB forms of TB require prolonged continuation phase
A.CNS (TB meningitis orTuberculoma)
B. Bone or joint TB (Vertebral (TB spondylitis), joint &
osteomyelitis.
 Regimen (a total of 12 months:2months intensive phase and10
months continuation phase); -2RHZE/10RH
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E. Adjuvant corticosteroid therapy
Adjuvant corticosteroid therapy, dexamethasone or
prednisolone tapered over 6- 8weeks should be used
for patients with the following two extra pulmonary
forms
 TB meningitis
 TB pericarditis
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Monitoring of patients on treatment
1. Clinical monitoring: During scheduled visit patient checked
for:
2. Persistence or reappearance of clinical feature of TB
Weight monitoring: weight is a useful indicator of
improvement Occurrence of Adverse drug reaction
Development of TB complication
Adherence: By reviewing the“ treatment supporter card” or
Unit TB register
Risk for drug resistance & need for drug susceptibility screen
test
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2. Bacteriologic monitoring for initially
bacteriologically confirmed PTB
 Sputum AFB should be done at end of 2nd,5th and
6th month of therapy.
 Molecular technique like Gene Xpert, MTB cannot
be used to monitor. WHY?
 Treatment as the technique may give false
positive result by identifying dead bacilli
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Bacteriologic monitoring…
 If AFB positive at the end of 2nd month: send sputum sample
for Xpert for DST.
 If at least Rifampicin sensitive: continue to the continuation
phase.
 If Rifampicin resistance: Mark as Rifampicin-resistant Tb &
the outcome is labeled as“ MDR TB”. Treatment will be
started as MDR-TB.
 If AFB is positive at the end of 5th or 6th month: the
outcome is treatment failure. DST testing and treatment
will proceed as MDR-TB suspect
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Treatmentof patients also infected with HIV
 All patients with HIV and active TB who are not on ART should be started
on ART as described below:
 CD4<50cells/mm3:InitiateART within 2weeks of starting TB t/t
 CD4 counts ≥50cells/mm: Initiate ART with in 8weeks of starting
TB treatment.
 During pregnancy, regardless of CD4 count: InitiateART as early as
feasible for to prevent HIV transmission to the infant.
 With TB meningitis: InitiateART after 8weeks of TB treatment.
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Nursing Management
 Promoting airway clearance
 Increasing the fluid intake promotes systemic hydration
 Nurse instructs the patient about correct positioning
 Promoting adherence to treatment regimen
 Understanding of the medications, schedule, and side effects,
avoiding alcohol consumption.
 Nurse educate the patient about regular drug taking,
 Taking medication on empty stomach or 1 hr. before meals.
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Cont--------- Promoting activity and adequate nutrition
 The nurse plans a progressive activity schedule that focuses on
increasing activity tolerance and muscle strength.
 A nutritional plan that allows for small, frequent meals may be
required.
 Liquid nutritional supplements may assist in meeting basic
caloric requirements
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Cont----- Preventing Transmission of TB Infection
 The nurse carefully instructs the patient about important
hygiene measures, including mouth care, covering the
mouth and nose when coughing and sneezing, proper
disposal of tissues, and hand hygiene.
 TB is a disease that must be reported to the health department
so that people who have been in contact with the affected
patient during the infectious stage ( Brunner textbook pdf 14th
edition)
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•Causes of Drug Resistant TB
Health care worker and Anti-TB medicine
programmatic factors
related factors
Patient related
factors
-Inappropriate or absent
guidelines
-Non- compliance with
guidelines
-Poor training and
supervision of HCWs
-Lack of anti- TB
treatment monitoring
-Poorly organised and/or
funded NTP
-Poor adherence (poor
DOT)
-Lack of information
on treatment
-Adverse events on
treatment
- Social barriers
(stigma, restrictions)
-Malabsorption due to
other causes
-Substance addiction
Mental disorder
-Poor quality
-Unavailability
-Poor storage
-Wrong dose or
inadequate
combination
Prevention and control of TB
• BCG at birth or first contact in first 1 year of
life(not to symptomatic HIV or children born to
sputum positive mothers)
• INH 10 mg/kg to children born to sputum positive
mothers. After 2 months do the Mantoux test. If
positive give full TB treatment, if negative continue
INH prophylaxis for 4 more months. Then BCG
• Contact tracing and investigation
• Active case finding
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Cont--------• Reducing overcrowding, stress, alcoholism
• Infection control – keeping windows open,
waiting n positive pressure ventilation, cough
etiquette, prompt health services to TB suspects,
separating TB cases and suspects from other
patients into a well ventilated area.
• Personal protection – N95 masks
• Health education
• Treatment of cases
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Complications
• Pleural effusion/empyema
• Pneumothorax
• Chronic obstructive pulmonary disease
• Cor pulmonale
• Extra pulmonary TB
Prognosis
• Good if PTB patient complies with treatment.
Fatal if untreated. Cure rate of MDR TB is 5060% at its best
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DDX TB
•
•
•
•
•
•
Bacterial pneumonia
Atypical pneumonia
Brucellosis
Bronchogenic carcinoma
Sorcoidosis
Hodgkin lymphoma
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ASTHMA
1
INTRODUCTION
 Asthma
is a chronic inflammatory disease of the
airways that causes airway hyper- responsiveness,
mucosal edema, and mucus production
Asthma is characterized by chronic air way
inflammation and increased airway hyperresponsiveness leading to symptoms of wheeze, cough,
chest tightness and dyspnoea.

Asthma is a disorder of thebronchial airways characterized by
period of reversible bronchospam.
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TYPES:
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ETIOLOGY:
Idiopathic
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ETIOLOGY AND RISK FACTOR
Asthma
occurs in families which suggest that it is an
inherited disorder.
 Allergy
is the strongest predisposing factor for
asthma.
 Chronic exposure to airway irritants or allergens
also increases the risk for developing asthma.
Common allergens can be seasonal (eg, grass, tree, and
weed pollens, mold, dust, or animal dander).
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Cont--- Excitatory
state (stress ,cry )
 Occupational environment factor
such as cold air, air pollution, infection,
 Occupational environment Other factor such as
cold air,air
pollution, infection, diet
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Cont-----Triggers
• Allergens
• Upper respiratory tract viral infections
• Exercise
• Cold air
• Sulfur dioxide Drugs ( BETA blockers aspirin)
• Stress
• Irritants (household sprays, paint fumes)
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CLASSIFICATION
Asthma is a complex disorder of the
conducting airways that most simply can be
classified as:
 extrinsic – implying a definite external cause
 intrinsic – when no causative agent can be
identified.
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PATHOPHYSIOLOGY:
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CLINICAL MANIFESTATIONS:
● Wheezing
● Cough
● Chest tightness
● Dyspone
● Hypoxia
● Nasal flaring
● Sputum is
thick and tenacious
● Decreased or absence of breath sounds called
“SILENT CHEST”
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SYMPTOMS:
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ASSESSMENT AND DIAGNOSTIC
STUDIES:
● History collection
● Physical examination
● Pulse oximetry
● Pulmonary function test
● Arterial blood gas
● Complete blood count
● Chest x-ray
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Cont------History taking
 A complete family, environmental, and
occupational history is essential.
 Family history : History of asthma in family
 Environmental history :
seasonal changes,
high pollen counts, mold, climate changes
(particularly cold air), and air pollution,
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CONTD…
Occupational history : occupation-related chemicals
and compounds, including metal salts, wood and
vegetable dust
 Medications (eg, aspirin)
 Industrial chemicals and plastics, biologic enzymes
(eg, laundry detergents), animal and insect dusts, sera,
and secretions.
Physical examination
 wheezing all over the lung
 breathlessness and cough.
 Cyanosis
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
INVESTIGATIONS
 Lung
function tests/ pulmonary function test
: Shows variable airflow limitation
 Blood tests :shows increase in the number of
eosinophils in peripheral blood (> 0.4 × 109/L).
 Sputum tests The presence of large numbers of
eosinophils in the sputum is a more useful
diagnostic tool.
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Cont------ Chest
X-ray : There are no diagnostic
features of asthma on the chest X-ray
A chest X-ray may be helpful in excluding a
pneumothorax, which can occur as a
complication of asthma
 Skin tests
Skin-prick tests (SPT) should be
performed in all cases of asthma to help
identify allergic causes.
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MANAGEMENT:
● Medications:
●
Bronchodilators:
-long acting beta adrenagic blockers:
eg:salmeterol,formeterol,theophylline
●
Anti-inflammatory drugs:
-corticosteriods:
eg:flunisolides,beclamethasone,cromolyn
-Mast cell stabilizers:
eg:montelukast,zileuton
●
DRY POWDER INHALERS
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CORTICOSTEROIDS ARE MOST
EFFECTIVE
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DELIVERY METHODS:
• Medications are typically provided as
metered-dose inhalers (MDIs) in combination
with an asthma spacer or as a dry powder
inhaler. The spacer is a plastic cylinder that
mixes the medication with air, making it
easier to receive a full dose of the drug. A
nebulizer may also be used.
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ADVERSE EFFECTS:
• Long-term use of inhaled corticosteroids at
conventional doses carries a minor risk of
adverse effects.Risks include the development
of cataracts and a mild regression in stature.
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OTHER METHODS:
● When
asthma is unresponsive to usual
medications, other options are available for both
emergency management and prevention of
flareups. For emergency management other
options include:
● Oxygen to alleviate hypoxia if saturations fall
below 92%.
● Oral corticosteroid are recommended with
five days of prednisone being the same 2
days of dexamethasone.
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Cont---● Magnesium
sulfate intravenous treatment has
been shown to provide a bronchodilating
effect when used in addition to other treatment
in severe acute asthma attacks.
● Heliox, a mixture of helium and oxygen,
may also be considered in severe
unresponsive cases
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NURSING MANAGEMENT:
➢ Check
vital signs at regular intervals.
➢ Monitor allergic symptoms.
➢ Administer medication, note action of
medications.
➢ Avoid exposure to pollution environment.
➢ Deep breathing exercises.
➢ Health education.
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NURSING DIAGNOSIS:
❖ Ineffective
airway cleareance related to
bronchospasm.
❖ Impaired breathing pattern related to excessive
mucus secretion.
❖ Sleep pattern disturbance related to cough and
dysponea.
❖ Anxiety related to difficulty in
breathing.
❖ Knowledge deficit related to treatment regimen.
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PLANNING AND GOALS
The major goals for the patient may include
 smoking cessation,
 Improved gas exchange, & Airway
clearance,
 improved breathing pattern,
 Improved activity tolerance ,
 Maximal self-management,
 Improved coping ability,
 Adherence to the therapeutic program ,Home care &
Absence of complications.
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PLANNING AND GOALS
 Assess
the client frequently, observing
respiratory rate and depth.
 Assess the breathing pattern for shortness of
breath, pursed-lip breathing, nasal flaring,
 Assess of Sternal and intercostals
retractions, or a prolonged expiratory,
phase.
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Cont-------- Place
the client in the fowler position
 Give oxygen by face mask as ordered.
 Give Nebulization using asthalin and impravent
solution.
 Monitor ABGs and oxygen saturation level to
determine the effectiveness of treatments.
 Reassure the patient .
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Differential Diagnosis of Asthma
•
•
•
•
•
•
•
•
•
•
•
Congestive heart failure
Myocardial infarction
Upper airway embolism
Foreign body aspiration
Tracheo bronchomalacia
Endobronchial lesion
Chronic obstructive pulmonary disease (copd)
Bronchiolitis
Vocal cord dysfunction
Hyperventilation syndrome
Acute bronchitis /pneumonia
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Reference
1.
Ethiopia tuberculosis roadmap overview, fiscal year 2022
2.
CDC U.S. TB Clinical Guidelines Update, 2022
3.
Final draft TBL-NSP July 2021 – June 2026, August 2020 by MOH
4.
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Acknowledgment
For WU Adult health Department
For Dr. Kumar & students
6/3/2023
By sani
165