Acute infective endocarditis with vegetations

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Acute infective endocarditis with vegetations
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Ventricular Aneurysm complicating MI
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Acutemyocardial infarction
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Left ventricular rupture complicating MI
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• Respiratory system
• Fatima Obeidat, MD

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1. Atelectasis
Body_ID HC013006
Body_ID P0481
Body_ID P013007
Body_ID F013002
Compression Atelectasis
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Figure 13-2 Various forms of atelectasis in adults.
Compression atelectasis (sometimes called passive or relaxation atelectasis) is usually associated with accumulations of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung. This is a frequent occurrence with pleural effusions, caused most commonly by congestive heart failure (CHF). Leakage of air into the pleural cavity (pneumothorax) also leads to compression atelectasis. Basal atelectasis resulting from the elevated position of the diaphragm commonly occurs in bedridden patients, in patients with ascites, and in patients during and after surgery.

• Also known as collapse, is loss of lung volume
  caused by inadequate expansion of airspaces.
• It results in shunting of inadequately oxygenated
  blood from pulmonary arteries into veins, thus
  giving rise to hypoxia.

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• On the basis of the underlying mechanism or the
  distribution of alveolar collapse, atelectasis is
  classified into three forms

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• A. Resorption atelectasis
• Occurs when total obstruction prevents air from
  reaching distal airways.
• The air already present gradually becomes
  absorbed, and alveolar collapse follows.

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• Causes
• 1.The most common cause is total obstruction of a
  bronchus by a mucous or mucopurulent plug, this
  frequently occurs postoperatively
• 2. but may also complicate bronchial asthma,
  chronic bronchitis,
• 3. or the aspiration of foreign bodies,
  particularly in children.

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• B. Compression Atelectasis
• sometimes called passive or relaxation
  atelectasis is usually associated with
  accumulations of fluid, blood, or air within the
  pleural cavity, which mechanically collapse the
  adjacent lung.

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• Causes
• 1. This is a frequent occurrence with pleural
  effusions
• 2. Leakage of air into the pleural cavity
  (pneumothorax).
• 3. Basal atelectasis resulting from the elevated
  position of the diaphragm commonly occurs in
  bedridden patients, in patients with ascites, and
  in patients during and after surgery.

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• C. Contraction (or cicatrization) atelectasis
• It occurs when either local or generalized
  fibrotic changes in the lung or pleura prevent
  expansion of the lung
• NOTE Atelectasis (except that caused by
  contraction) is potentially reversible and should
  be treated promptly to prevent hypoxemia and
  superimposed infection of the collapsed lung.

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• ACUTE LUNG INJURY
• The term acute lung injury encompasses a spectrum
  of pulmonary lesions (endothelial and
  epithelial), which can be initiated by numerous
  conditions.
• Clinically, acute lung injury manifests as

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• (1) the acute onset of dyspnea,
• (2) decreased arterial oxygen pressure
  (hypoxemia),
• (3) development of bilateral pulmonary
  infiltrates on radiographs,
• (4) absence of clinical evidence of primary
  left-sided heart failure.

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• Since the pulmonary infiltrates in acute lung
  injury are usually caused by damage to the
  alveolar capillary membrane rather than
  left-sided heart failure , they represent an
  example of noncardiogenic pulmonary edema.
• Acute lung injury can progress to the more severe
  acute respiratory distress syndrome,

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• Acute Respiratory Distress Syndrome (ARDS)
• ARDS is a clinical syndrome caused by diffuse
  alveolar capillary and epithelial damage.
• There is usually rapid onset of life-threatening
  respiratory insufficiency, cyanosis, and severe
  arterial hypoxemia that is refractory to oxygen
  therapy and that may progress to multisystem
  organ failure.

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• The histologic manifestation of ARDS in the lungs
  is known as diffuse alveolar damage.
• ARDS can occur in a multitude of clinical
  settings and is associated with either direct
  injury to the lung or indirect injury in the
  setting of a systemic process .

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• - Direct causes
• Pneumonia
• Aspiration of gastric contents
• -Indirect cause
• Pancreatitis
• Septic Shock

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Morphology

• In the acute phase of ARDS
• Microscopically, there is
• necrosis of alveolar epithelial cells,
• interstitial and intra-alveolar edema and
  hemorrhage, and (particularly with sepsis)
  collections of neutrophils in capillaries.

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• The most characteristic finding is the presence
  of hyaline membranes, particularly lining the
  distended alveolar ducts .
• - Such membranes consist of fibrin-rich edema
  fluid admixed with remnants of necrotic
  epithelial cells.

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• In the organizing stage there is
• marked proliferation of type II pneumocytes in an
  attempt to regenerate the alveolar lining.
• Resolution is unusual more commonly there is
  organization of the fibrin exudates, with
  resultant intra-alveolar fibrosis.

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• Clinical Course
• Approximately 85 of patients develop the
  clinical syndrome of acute lung injury or ARDS
  within 72 hours of the initiating insult.
• Despite improvements in supportive therapy the
  mortality rate among ARDS cases seen yearly is
  still about 60.

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• Predictors of poor prognosis in ARDS include
• advanced age,
• underlying bacteremia (sepsis),
• and the development of multisystem (especially
  cardiac, renal, or hepatic) failure.

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• If the patient survive the acute stage, diffuse
  interstitial fibrosis may occur and continue to
  compromise respiratory function.
• However, in most patients who survive the acute
  insult and are spared the chronic sequela, normal
  respiratory function returns within 6 to 12
  months