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Pemicu 3

Bronchiectasis and tuberculosis are two common chronic cough conditions. Bronchiectasis is an abnormal permanent dilatation of the bronchi caused by inflammation and destruction of the bronchial wall, usually due to infection. It can be focal or diffuse. Three patterns are cylindrical, varicose, and saccular bronchiectasis. In tuberculosis, the bacteria Mycobacterium tuberculosis is usually transmitted via airborne droplets and forms granulomas in the lungs. Primary tuberculosis involves the lungs and lymph nodes while postprimary tuberculosis reactivates from latent infection in the upper lobes. Both conditions can cause chronic cough with sputum production.

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31 views37 pages

Pemicu 3

Bronchiectasis and tuberculosis are two common chronic cough conditions. Bronchiectasis is an abnormal permanent dilatation of the bronchi caused by inflammation and destruction of the bronchial wall, usually due to infection. It can be focal or diffuse. Three patterns are cylindrical, varicose, and saccular bronchiectasis. In tuberculosis, the bacteria Mycobacterium tuberculosis is usually transmitted via airborne droplets and forms granulomas in the lungs. Primary tuberculosis involves the lungs and lymph nodes while postprimary tuberculosis reactivates from latent infection in the upper lobes. Both conditions can cause chronic cough with sputum production.

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kheluwis
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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LO 1

Macam-macam batuk kronik

Bronkiektasis
Bronchiectasis is an abnormal and
permanent dilatation of bronchi.
It may be either focal, involving
airways supplying a limited region of
pulmonary parenchyma, or diffuse,
involving airways in a more
widespread distribution.

Three different patterns of bronchiectasis


have been described:
cylindrical bronchiectasis, the involved bronchi
appear uniformly dilated and end abruptly at
the point that smaller airways are obstructed
by secretions.
varicose bronchiectasis, the affected bronchi
have an irregular or beaded pattern of
dilatation resembling varicose veins.
saccular (cystic) bronchiectasis, the bronchi
have a ballooned appearance at the periphery

The bronchial dilatation of bronchiectasis is


associated with destructive and
inflammatory changes in the walls of
medium-sized airways, often at the level of
segmental or subsegmental bronchi.
As a result of the inflammation, vascularity
of the bronchial wall increases, with
associated enlargement of the bronchial
arteries and anastomoses between the
bronchial and pulmonary arterial circulations.

Patogenesis dan etiologi


Bronchiectasis is a consequence of
inflammation and destruction of the
structural components of the
bronchial wall.
Infection is the usual cause of the
inflammation; microorganisms such
as Pseudomonas aeruginosa and
Haemophilus influenzae

Manifestasi Klinis
Patients typically present with
persistent or recurrent cough and
purulent sputum production
Hemoptysis, Dyspnea, wheezing
Any combination of crackles, rhonchi,
and wheezes may be heard, all of
which reflect the damaged airways
containing significant secretions.

Radiographic and Laboratory


Findings
The findings are often nonspecific
patients with saccular bronchiectasis may
have prominent cystic spaces either with
or without air-liquid levels
Other findings are due to dilated airways
with thickened walls:
When seen longitudinally, the airways appear
as "tram tracks"
when seen in cross-section, they produce
"ring shadows."

Histoplasmosis

In most endemic areas, H. capsulatum var.


capsulatum is the causative agent; in Africa, H.
capsulatum var. duboisii is also found.
Myceliathe naturally infectious form of
Histoplasmahave a characteristic appearance,
with microconidial and macroconidial forms.
Microconidia are oval and are small enough (25
m) to reach the terminal bronchioles and alveoli.
After infecting the host, mycelia transform into
the yeasts that are found inside macrophages
and other phagocytes.

Epidemiologi
Histoplasmosis is the most prevalent endemic
mycosis in North America.
Its endemicity is particularly notable in certain
parts of North, Central, and South America;
Africa; and Asia.
Soil enriched with bird or bat droppings promotes
the growth and sporulation of Histoplasma.
Activities associated with high-level exposure
include spelunking, excavation, cleaning of
chicken coops, demolition and remodeling of old
buildings, and cutting of dead trees.

Patogenesis
Infection follows inhalation of microconidia
Once they reach the alveolar spaces, microconidia
are rapidly engulfed by alveolar macrophages.
The microconidia transform into budding yeasts
The yeasts are capable of growing and multiplying
inside resting macrophages.
Before the development of cellular immunity,
yeasts use the phagosomes as a vehicle for
translocation to local draining lymph nodes,
whence they spread hematogenously throughout
the reticuloendothelial system.

In the immunocompetent host, the immune


cells form granulomas that contain the
organisms.
These granulomas typically fibrose and calcify
In patients with impaired cellular immunity, the
infection is not contained and can disseminate.
Progressive disseminated histoplasmosis (PDH)
can involve multiple organs, most commonly
the bone marrow, spleen, liver, adrenal glands,
and mucocutaneous membranes.

Clinical Manifestations
fever, chills, sweats, headache, myalgia,
anorexia, cough, dyspnea, and chest pain.
Chest radiographs show signs of
pneumonitis with hilar or mediastinal
adenopathy
In healed histoplasmosis, calcified
mediastinal nodes or lung parenchyma
may erode through the walls of the airways
and cause hemoptysis. This condition is
called broncholithiasis.

Diagnosis
Fungal culture remains the gold standard
diagnostic test for histoplasmosis
Fungal stains of cytopathology or biopsy
materials showing Histoplasma yeasts
PDH
The detection of Histoplasma antigen in
body fluids is extremely useful in the
diagnosis of PDH and acute diffuse
pulmonary histoplasmosis.

LO 2
TBC

TBC
Caused by bacteria of the Mycobacterium
tuberculosis complex, usually affects the
lungs, although other organs are involved
in up to one-third of cases.
If untreated, the disease may be fatal
within 5 years in 5065% of cases.
Transmission usually takes place through
the airborne spread of droplet nuclei
produced by patients with infectious
pulmonary tuberculosis.

Mycobacteria belong to the family


Mycobacteriaceae and the order
Actinomycetales.
Agent of human disease is M.
tuberculosis. rod-shaped, non-sporeforming, thin aerobic bacterium
measuring 0.5 m by 3 m

The complex includes :


M. bovis (resistant to pyrazinamide, once an important
cause of tuberculosis transmitted by unpasteurized milk),
M. caprae (related to M. bovis),
M. africanum (isolated from cases in West, Central, and
East Africa),
M. microti (the "vole" bacillus, a less virulent and rarely
encountered organism),
M. pinnipedii (a bacillus infecting seals and sea lions in the
southern hemisphere and recently isolated from humans)
M. canettii (a rare isolate from East African cases that
produces unusual smooth colonies on solid media and is
considered closely related to a supposed progenitor type).

Patogenesis
The interaction of M. tuberculosis with the
human host begins when droplet nuclei
containing microorganisms from infectious
patients are inhaled.
Majority of inhaled bacilli are trapped in the
upper airways and expelled by ciliated
mucosal cells, a fraction (usually <10%)
reach the alveoli.
There, alveolar macrophages that have not
yet been activated phagocytize the bacilli

If the bacilli are successful in


arresting phagosome maturation,
then replication begins and the
macrophage eventually ruptures and
releases its bacillary contents.
Granulomatous lesions (tubercles)
are formed.

Activated macrophages aggregate around


the lesion's center and effectively neutralize
tubercle bacilli without causing further
tissue destruction.
In the central part of the lesion, the necrotic
material resembles soft cheese (caseous
necrosis)
Even when healing takes place, viable bacilli
may remain dormant within macrophages or
in the necrotic material for many years.

Pulmonary Tuberculosis
Pulmonary tuberculosis can be
categorized as primary or
postprimary (secondary)

Primary Disease
Primary pulmonary tuberculosis occurs soon after the
initial infection with tubercle bacilli.
The lesion forming after infection is usually peripheral
and accompanied in more than half of cases by hilar or
paratracheal lymphadenopathy, which may not be
detectable on chest radiography.
The lesion heals spontaneously and may later be evident
as a small calcified nodule (Ghon lesion).
Pleural effusion, results from the penetration of bacilli
into the pleural space from an adjacent subpleural focus.
In severe cases, the primary site rapidly enlarges, its
central portion undergoes necrosis, and cavitation
develops

Enlarged lymph nodes may compress bronchi,


causing obstruction and subsequent segmental or
lobar collapse.
Partial obstruction may cause obstructive
emphysema, and bronchiectasis may also develop.
Bacilli reach the bloodstream from the pulmonary
lesion or the lymph nodes and disseminate into
various organs, where they may produce
granulomatous lesions.
immunocompromised persons may develop miliary
tuberculosis and/or tuberculous meningitis.

Postprimary Disease
Also called adult-type, reactivation, or
secondary tuberculosis,
results from endogenous reactivation of latent
infection and is usually localized to the apical
and posterior segments of the upper lobes
Massive involvement of pulmonary segments
or lobes, produces tuberculous pneumonia.
Some pulmonary lesions become fibrotic and
may later calcify, but cavities persist in other
parts of the lungs.

Symptoms and signs are often nonspecific and


insidious: fever and night sweats, weight loss,
anorexia, malaise, and weakness.
Cough often initially nonproductive and subsequently
accompanied by the production of purulent sputum,
sometimes with blood streaking.
Massive hemoptysis may ensue as a consequence of
the erosion of a blood vessel in the wall of a cavity.
Pleuritic chest pain sometimes develops in patients
with subpleural parenchymal lesions.
Extensive disease may produce dyspnea and, in rare
instances, adult respiratory distress syndrome (ARDS).

Miliary or Disseminated Tuberculosis


Miliary tuberculosis is due to hematogenous
spread of tubercle bacilli.
Fever, night sweats, anorexia, weakness,
and weight loss are presenting symptoms in
the majority of cases.
Hepatomegaly, splenomegaly, and
lymphadenopathy.
Eye examination may reveal choroidal
tubercles
Meningismus

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