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fatty material thickens, hardens (forms calcium deposits), and may eventually block the arteries.
Atherosclerosis is a type of arteriosclerosis. The two terms are often used to mean the same
thing.
Causes
Atherosclerosis is a common disorder that specifically affects the medium and large arteries. It
occurs when fatfat, cholesterol, and other substances build up in the walls of arteries and form
hard structures called plaques.
Eventually, the plaques can make the artery narrow and less flexible, making it harder for blood
to flow. If the coronary arteries become narrow, blood flow to the heart can slow down or stop.
This can cause chest pain (stable anginastable angina), shortness of breath, heart attackheart
attack, and other symptoms.
Pieces of plaque can break off and move through the affected artery to smaller blood vessels,
blocking them and causing tissue damage or death (embolization). This is a common cause of
heart attack and stroke. Blood clots can also form around a tear (fissure) in the plaque leading to
blocked blood flow. If the clot moves into an artery in the heart, lungs, or brain, it can cause a
stroke, heart attack, or pulmonary embolism. In some cases, the atherosclerotic plaque is
associated with a weakening of the wall of an artery leading to an aneurysm.
• DiabetesDiabetes
• Heavy alcohol use
• High blood pressure
• High blood cholesterolHigh blood cholesterol levels
• High-fat diet
• Increasing age
• ObesityObesity
• Personal or family history of heart diseaseheart disease
• Smoking
Atherosclerosis can affect many different organ systems, including the heart, lungs, brain,
intestines, kidneys, and limbs (extremities).
Symptoms
Symptoms
Symptoms usually do not occur until blood flow becomes restricted or blocked.
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Pathophysiology
Gastric contents produce damage mainly from gastric acid, although food and
other ingested material (eg, activated charcoal as in treatment of overdose) are
injurious in quantity. Gastric acid causes a chemical burn of the airways and lung
leading to rapid bronchoconstriction, atelectasis, edema, and alveolar
hemorrhage. Symptoms include acute dyspnea with cough that is sometimes
productive of pink frothy sputum, tachypnea, tachycardia, fever, diffuse crackles,
and wheezing. Chest x-ray shows diffuse infiltrates frequently but not
exclusively in dependent segments, while pulse-oximetry and ABGs demonstrate
hypoxemia. Treatment is supportive, often involving supplemental O2 and
mechanical ventilation. Antibiotics often are given to patients with witnessed or
known gastric aspiration. The syndrome may resolve spontaneously, usually
within a few days, or may progress to acute respiratory distress syndrome.
Sometimes bacterial superinfection occurs.
Anaerobes often can be cultured from sputum, but it is unclear whether they are
primary infecting organisms to which treatment should be directed or whether
they are simply one of several organisms causing infection.
Symptoms and signs of pneumonia and abscess are similar and include chronic
low-grade dyspnea, fever, weight loss, and cough productive of putrid, foul-
tasting sputum. Patients may have signs of poor oral hygiene.
Diagnosis
Chest x-ray shows an infiltrate, frequently but not exclusively, in the dependent
lung segments, ie, the superior or posterior basal segments of a lower lobe or the
posterior segment of an upper lobe.
Treatment
Pathophysiology
Aspiration causes an inflammatory reaction called pneumonitis. This can result in damage to the
lung parenchyma. Damage to lung parenchyma causes an inflammatory reaction that can lead to
symptoms such as fever, cough or elevation of white cell count. A secondary bacterial infection
can occur owing to this damaged parenchyma leading to aspiration pneumonia.
The basal segments of the lower lobes are more commonly affected in a patient who aspirates
while sitting upright. [2] The posterior segments of the upper lobes or the apical segments of the
lower lobes are affected in a patient who aspirates while recumbent.
Pathophysiology Concepts
Aspiration is the introduction of a foreign substance into the lungs, but the mere instillation of
foreign substance into the subglottic airway is not sufficient to produce disease. Damage to the
pulmonary tree, which ranges from mild to fatal, depends on the nature, volume and pH of the
aspirated contents, and the pathogenicity of the organisms. Physiologic changes resulting from
aspiration of acidic fluid or gastric contents include a decline in arterial blood oxygen tension,
increased alveolar capillary membrane permeability, and a decrease in intravascular volume. The
lungs can become edematous and gas exchange abnormalities are the result. Histologic
examination shows tracheal mucosal desquamation, damage to the cells of the alveolar lining and
capillary inflammation 24 to 36 hours after aspiration.
Gastric acid aspirant results in chemical burns that destroy alveoli, which results in acute onset of
respiratory distress secondary to widespread bronchospasm, hypoxemia, and parenchymal
infection. The lower the pH (less than or equal to 2.5) the more severe the injury. There is a 30%
incidence of subsequent development of adult respiratory distress syndrome (ARDS) after acidic
aspiration.
Normally, micro-aspirates are cleared by several mechanisms or lines of defense. The materials
are entrapped and removed by filtration, coughing, or by action of the cilia. At the cellular level,
the immune system clears by using inactivation, IgA antibodies, or opsonization, and subsequent
phagocytosis. Loss of these defense mechanisms results in infection and colonization by
pathogenic organisms.
Clinical Manifestations