pulmonary vascular disease and atelectasis Flashcards

(29 cards)

1
Q

What is the most common cause of pulmonary embolism?

A

Deep vein thrombosis (DVT) of the lower extremity.

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2
Q

What are risk factors for pulmonary embolism?

A

Immobility, CHF, surgery, trauma, oral contraceptives, malignancy, hypercoagulability disorders.

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3
Q

What are consequences of pulmonary arterial occlusion?

A

Increased pulmonary artery pressure and ischemia of affected lung.

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4
Q

What causes hypoxemia in pulmonary embolism?

A

Perfusion of atelectatic lung zones, decreased cardiac output, and right-to-left shunting.

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5
Q

What is a saddle embolus?

A

A large embolus lodged at the bifurcation of the pulmonary artery.

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6
Q

What can large emboli cause?

A

Sudden death, acute cor pulmonale, diminished cardiac output.

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7
Q

What are clinical features of pulmonary embolism?

A

Dyspnea, tachypnea, tachycardia, pleuritic chest pain, sudden death.

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8
Q

What are diagnostic tools for PE?

A

CT angiogram (gold standard), VQ scan, echocardiogram, D-dimer, Doppler ultrasound.

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9
Q

What is the diagnostic threshold for pulmonary hypertension?

A

Pulmonary artery pressure ≥ 25 mm Hg at rest.

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10
Q

What are causes of secondary pulmonary hypertension?

A

Left heart failure, thromboemboli, chronic lung disease.

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11
Q

What mutation is seen in idiopathic pulmonary hypertension?

A

BMPR2 gene mutation.

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12
Q

What vascular changes occur in pulmonary hypertension?

A

Atheromas, medial wall thickening, intimal fibrosis, plexiform lesions.

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13
Q

What are symptoms of primary pulmonary hypertension?

A

Fatigue, syncope, dyspnea on exertion, cyanosis, chest pain.

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14
Q

What are treatment options for primary pulmonary hypertension?

A

Vasodilators, lung transplant.

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15
Q

What triad is common in alveolar hemorrhagic syndromes?

A

Hemoptysis, anemia, diffuse pulmonary infiltrates.

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16
Q

What are examples of alveolar hemorrhage syndromes?

A

Goodpasture syndrome, Wegener’s granulomatosis, idiopathic pulmonary hemosiderosis.

17
Q

What is the pathogenesis of Goodpasture syndrome?

A

Autoantibodies against α3 chain of collagen IV causing basement membrane destruction.

18
Q

What are histological findings in Goodpasture syndrome?

A

Intra-alveolar hemorrhage, hemosiderin, patchy necrosis, septal thickening.

19
Q

What is the treatment for Goodpasture syndrome?

A

Plasmapheresis, immunosuppressants, renal transplant.

20
Q

How does idiopathic pulmonary hemosiderosis differ from Goodpasture?

A

Similar lung findings but no renal involvement or anti-BM antibodies.

21
Q

What is atelectasis?

A

Incomplete lung expansion or collapse of previously inflated lung.

22
Q

What are the three types of atelectasis?

A

Resorption, compression, contraction.

23
Q

What causes resorption atelectasis?

A

Airway obstruction from secretions, exudates, tumors, foreign bodies.

24
Q

What are clinical signs of resorption atelectasis?

A

Ipsilateral mediastinal shift, absent breath sounds, decreased lung movement.

25
What causes compression atelectasis?
Air, fluid, or tumor in pleural cavity exerting pressure on lung.
26
What are examples of compression atelectasis?
Tension pneumothorax, pleural effusion.
27
What clinical feature is seen in compression atelectasis?
Mediastinum shifts away from the affected side.
28
What causes contraction atelectasis?
Pulmonary or pleural fibrosis preventing full lung expansion.
29
Is atelectasis reversible?
Yes, except when caused by contraction; early treatment prevents infection and hypoxemia.