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PATHOPHYSIOLOGY

PNEUMONIA
Pneumonia is often preceded by an upper respiratory viral
infection, aspiration of phlegm or gastric contents, asthma, or exposure
to allergens or irritants. It is an infection that inflames the air sacs in
one or both lungs. The air sacs may fill with fluid or pus (purulent
material), causing cough with phlegm or pus, fever, chills, and difficulty
breathing.
A variety of organisms, including bacteria, viruses and fungi, can
cause pneumonia. Pneumonia can range in seriousness from mild to
life-threatening. It is most serious for infants and young children,
people older than age 65, and people with health problems or
weakened immune systems.

Pathophysiology of Pneumonia
Any infectious organisms that reach the alveoli are likely to be
highly virulent, as they have already evaded the host’s physical defense
mechanisms. Consequently, they may overwhelm the macrophages,
resulting in production of a fibrin-rich exudate that fills the infected and
neighboring alveolar spaces, causing them to stick together, rendering
them airless (Driver, 2012). The inflammatory response also results in a
proliferation of neutrophils. This can damage lung tissue, leading to
fibrosis and pulmonary edema, which also impairs lung expansion.
The inflammatory response can also lead to the development of a
pleural effusion which is thought to complicate up to 40% of cases of
pneumonia (Koegelenberg et al, 2008 in Driver, 2012). These changes
result in reduced gaseous exchange. As a result, vital organs become
oxygen deprived and the respiratory effort required with each breath
will be increased as a result of the disturbance in normal physiology.
Respiratory and heart rate will increase in response to falling oxygen
and rising carbon dioxide levels.
There is an intricate balance between the organisms residing in
the lower respiratory tract and the local and systemic defense
mechanisms (both innate and acquired) which when disturbed gives
rise to inflammation of the lung parenchyma, i.e., pneumonia. Common
defense mechanisms that are compromised in the pathogenesis of
pneumonia include:
 Systemic defense mechanisms like humoral and
complement-mediated immunity that is compromised in
diseases like common variable immunodeficiency (CVID), X-
linked agammaglobulinemia (inherited), and functional
asplenia (acquired). Impaired cell-mediated immunity
predisposes individuals to infection by intracellular
organisms like viruses and organisms of low virulence
like Pneumocystis pneumonia (PJP), fungal causes, among
others.
 The mucociliary clearance that is often impaired in cigarette
smokers, post-viral state, Kartergerner syndrome, and other
related conditions.
 Impaired cough reflex seen in comatose patients, certain
substances of abuse.
 Accumulation of secretions as seen in cystic fibrosis or
bronchial obstruction.
The resident macrophages serve to protect the lung from foreign
pathogens. Ironically, the inflammatory reaction triggered by these
very macrophages is what is responsible for the histopathological and
clinical findings seen in pneumonia. The macrophages engulf these
pathogens and trigger signal molecules or cytokines like TNF-a, IL-8, and
IL-1 that recruit inflammatory cells like neutrophils to the site of
infection. They also serve to present these antigens to the T cells that
trigger both cellular and humoral defense mechanisms, activate
complement and form antibodies against these organisms. This, in
turn, causes inflammation of the lung parenchyma and makes the lining
capillaries "leaky," which leads to exudative congestion and underlines
the pathogenesis of pneumonia.
The signs and symptoms of pneumonia vary from mild to severe,
depending on factors such as the type of germ causing the infection,
and your age and overall health. Mild signs and symptoms often are
similar to those of a cold or flu, but they last longer.
Signs and symptoms of pneumonia may include:
 Chest pain when you breathe or cough
 Confusion or changes in mental awareness (in adults age 65
and older)
 Cough, which may produce phlegm
 Fatigue
 Fever, sweating and shaking chills
 Lower than normal body temperature (in adults older than
age 65 and people with weak immune systems)
 Nausea, vomiting or diarrhea
 Shortness of breath

TUBERCULOSIS
Tuberculosis (TB) is a chronic, progressive mycobacterial infection,
often with a period of latency following initial infection. TB is an
airborne disease caused by the bacterium Mycobacterium tuberculosis
(M. tuberculosis).
Tuberculosis is caused by bacteria that spread from person to
person through microscopic droplets released into the air. This can
happen when someone with the untreated, active form of tuberculosis
coughs, speaks, sneezes, spits, laughs or sings.
Although tuberculosis is contagious, it's not easy to catch. You're
much more likely to get tuberculosis from someone you live with or
work with than from a stranger. Most people with active TB who've had
appropriate drug treatment for at least two weeks are no longer
contagious.

Pathophysiology of Tuberculosis
Infection occurs when a person inhales droplet nucleus containing
tubercle bacilli that reach the alveoli of the lungs. These tubercle bacilli
are ingested by alveolar macrophages; the majority of these bacilli are
destroyed or inhibited. A small number may multiply intracellularly and
are released when the macrophages die.
If alive, these bacilli may spread by way of lymphatic channels or
through the bloodstream to more distant tissues and organs (including
areas of the body in which TB disease is most likely to develop: regional
lymph nodes, apex of the lung, kidneys, brain, and bone). This process
of dissemination primes the immune system for a systemic response.
The first contact of the Mycobacterium organism with a host leads
to manifestations known as primary tuberculosis. This primary TB is
usually localized to the middle portion of the lungs, and this is known as
the Ghon focus of primary TB. In most infected individuals, the Ghon
focus enters a state of latency. This state is known as latent
tuberculosis.
Latent tuberculosis is capable of being reactivated after
immunosuppression in the host. A small proportion of people would
develop an active disease following first exposure. Such cases are
referred to as primary progressive tuberculosis. Primary progressive
tuberculosis is seen in children, malnourished people, people with
immunosuppression, and individuals on long-term steroid use.
Most people who develop tuberculosis, do so after a long period
of latency (usually several years after initial primary infection). This is
known as secondary tuberculosis. Secondary tuberculosis usually occurs
because of reactivation of latent tuberculosis infection. The lesions of
secondary tuberculosis are in the lung apices. A smaller proportion of
people who develop secondary tuberculosis does so after getting
infected a second time (re-infection).
The lesions of secondary tuberculosis are similar for both
reactivation and reinfection in terms of location (at the lung apices),
and the presence of cavitation enables a distinction from primary
progressive tuberculosis which tends to be in the middle lung zones and
lacks marked tissue damage or cavitation.
Although your body may harbor the bacteria that cause
tuberculosis (TB), your immune system usually can prevent you from
becoming sick. For this reason, doctors make a distinction between:
Latent TB. In this condition, you have a TB infection, but the
bacteria remain in your body in an inactive state and cause no
symptoms. Latent TB, also called inactive TB or TB infection, isn't
contagious. It can turn into active TB, so treatment is important for the
person with latent TB and to help control the spread of TB. An
estimated 2 billion people have latent TB. Active TB. This condition
makes you sick and in most cases can spread to others. It can occur in
the first few weeks after infection with the TB bacteria, or it might
occur years later.
Signs and symptoms of active TB include:
 Coughing that lasts three or more weeks.
 Coughing up blood.
 Chest pain, or pain with breathing or coughing.
 Unintentional weight loss.
 Fatigue
 Fever
 Night sweats
 Chills
 Loss of appetite

SOURCE:
https://lms.rn.com/courses/1777/index.html?
jmptopg=pathophysiology_of_pneumonia.html
https://www.ncbi.nlm.nih.gov/books/NBK526116/
https://www.mayoclinic.org/diseases-
conditions/pneumonia/symptoms-causes/syc
https://www.ncbi.nlm.nih.gov/books/NBK441916/
https://www.google.com/url?
sa=t&source=web&rct=j&url=https://www.cdc.gov/tb/education/corec
urr/pdf/chapter2.pdf&ved=2ahUKEwiOusWf59TsAhUMZt4KHV5NAew
QFjABegQIBRAF&usg=AOvVaw0S6Dal-CPvEXvsPp2GHtWP
https://www.mayoclinic.org/diseases-
conditions/tuberculosis/symptoms-causes/syc-20351250

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