Path - Lecture 4 (pulomary Vascular Diseases ) Flashcards

1
Q

Pulmonary Thromboembolism

A

-DVT related

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2
Q

The pathophysiologic consequences of pulmonary thromboembolism depend largely on:

A
  1. The size of the embolus
    2.the cardiopulmonary status of the patient
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3
Q

two important consequences of pulmonary arterial occlusion:

A

1.an increase in pulmonary artery pressure from blockage of flow and
2.Ischemia of the downstream pulmonary parenchyma

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4
Q

Pathogenesis of pulmonary thromboembolism

A

1.Perfusion of atelectatic lung zones

2.The decrease in cardiac output causes a widening of the difference in arterial-venous oxygen saturation.

3.Right-to-left shunting of blood may occur through a patent foramen ovale

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5
Q

Morphology of pulmonary embolism - large embolus

A

-large embolus may embed in the pulmonary artery
-it may also lodge in the major branches or lodge astride the bifurcation as a saddle embolus
-increase in pulmonary artery pressure
-right sided heart failure

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6
Q

Morphology of pulmonary thromboembolism In small vessels

A

-impact medium sized and small sized pulmonary arteries
-hemorrhage may occur as a result of ischemic damage to the endothelial cells (leading to capillary rupture).
-With compromised cardiovascular status (congestive heart failure or underlying lung disease) infarction results.

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7
Q

Pulmonary embolism clinical features

A

-dyspnea
-tachypnea
-tachycardia
-pleuritic chest pain
-chronic cor pulmonale

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8
Q

Pulmonary Hypertension

A

Pulmonary artery pressure greater than or equal to 25 mm Hg at rest

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9
Q

What are the classifications of pulmonary HTN

A

-LVF and mitral stenosis
-recurrent tiny thromboembolism
-COPD ,Brochiectasis ,ILD
-idiopathic

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10
Q

Pathogenesis of idiopathic pulmonary htn

A

-inactivating germ line mutations in
the gene encoding bone morphogenetic
protein receptor 2 (BMPR2)
-Defects in BMPR2 signaling leads to dysfunction of endothelium and proliferation of vascular smooth muscle cells in the pulmonary vasculature

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11
Q

Morphology of pulmonary htn

A

-medium sized arteries walls thicken
-Small arteries/arterioles = Thickening, medial hypertrophy, reduplication of
the internal and external elastic lamina
-RV hypertrophy
-plexiform lesions

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12
Q

Clinical features of primary pulmonary htn

A

• Young women
• Fatigue, syncope, dyspnea on exertion, chest pain
• Severe respiratory insufficiency, cyanosis, death from right heart failure 2-5 years from diagnosis

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13
Q

Clinical features of secondary pulmonary htn

A

• Any age onset
• Reflects underlying disease (pulmonary or cardiovascular)
• Symptoms of respiratory insufficiency and right heart strain

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14
Q

Diffuse Alveolar Haemorrhage Syndromes

A

Immune mediated diseases which manifest as :
Hemoptyisis , anemia ,diffuse pulmonary infiltrates
-good pasture syndrome
-Wegners granulomatosis
-idiopathic hemosiderosis

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15
Q

GOODPASTURE SYNDROME - epidemiology

A

-Pulmonary-renal syndrome: proliferative and rapidly progressive
glomerulonephritis and hemorrhagic interstitial pneumonitis
- teens and 20s
-males
-

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16
Q

Pathogenesis of good pastures syndrome

A

• Kidney and lung injury are caused by circulating autoantibodies against the non-collagenous domain of the α3 chain of collagen IV.
• The antibodies initiate inflammatory destruction of the basement membrane in renal glomeruli and pulmonary alveoli
• Linear deposition of IgG along basement membranes – glomerular basement membranes (kidney) or alveolar septa (lung)

17
Q

Morphology of good pasture

A

-gross : heavy lungs , red consolidation
-micro :
-Intra-alveolar hemorrhage
• Patchy necrosis of alveolar walls
• Intra-alveolar hemosiderin
• Septal thickening and reactive hypertrophy of type II cells

18
Q

Clinical findings in good pastures

A

-Hemoptysis,anemia,pulmonaryinfiltrates
• Featuresofglomerulonephritis–hematuria,edema,uremia
-focal consolidations
-linear deposits of Ig along the basement membrane

19
Q

Idiopathic pulmonary hemosiderosis

A

-children >adults
-histo similar to good pastures
-no association with renal disease
-no anti BM antibody

20
Q

Acquired atelectasis

A

-Refers either to incomplete expansion of the lungs (neonatal atelectasis) or to the collapse of previously inflated lungs
-decreased oxygenation
-ventilation perfusion imbalance

21
Q

RESORPTION ATELECTASIS

A

-stems from obstruction of an airway
-excessive secretions in the smaller bronchi
-Aspiration of foreign bodies
-Intrabronchial tumors

22
Q

Clinical features of resorption atelectasis

A

• Ipsilateral deviation of trachea and mediastinum
• Ipsilateral diaphragmatic elevation
• Absent breath sounds and absent
vocal vibratory sensation (tactile
fremitus)
• Collapsed lung does not expand on
inspiration

23
Q

Compression Atelectasis

A

-compressed by air ,fluid or tumor
-accumulate in the pleural cavity and increases pressure
-Trachea and mediastinum shift away from the affected lung

24
Q

Contraction atelectasis

A

-Occurs when focal or generalized pulmonary or pleural fibrosis prevents full lung expansion

25
Q

Course and complications of atelectasis

A

-is usually reversible
-treat promptly