pulmonaryarterial.txt

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Author:
arimoses
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52106
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pulmonaryarterial.txt
Updated:
2010-11-28 22:31:10
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pulmonary
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pulmonary
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  1. What is the diagnostic feature of acute pulmonary infarct?
    Ischemic necrosis of lung within area of hemorrhage.
  2. Pulmonary blood pressure is usually __ of systemic blood pressure?
    1/8.
  3. Pulmonary hypertension is most frequently secondary to?
    Conditions that increase pulmonary blood flow, pressure, resistance, or left heart resistance to blood flow.
  4. Name some causes of pulmonary hypertension?
    • COPD, interstitial lung diseases
    • CHF
    • Recurrent PE
    • congenital or acquired heart diseases
    • Primary or idiopathic - most common in young women.
  5. What is the pathogenesis of pulmonary hypertension?
    Pulmonary endothelial cell and/or vascular smooth muscle dysfunction.
  6. What is bone morphogenetic protein receptor type 2 (BMPR2), and how does it affect pulmonary hypertension?
    • A cell surface receptor that binds to several ligands of teh TGF-B pathway and has inhibitory effects on proliferation
    • Loss of function mutation of gene leads to vascular endothelial and pulmonary smooth muscle proliferation.
  7. How does Serotonin transporter gene (5-HTT) affect pulmonary hypertension?
    Polymorphisms lead to enhanced expression on vascular smooth muscle and proliferation.
  8. The diffuse alveolar hemorrhage syndromes present with the triad of?
    • Hemoptysis
    • Anemia
    • Diffuse pulmonary infiltrates.
  9. What are the three diffuse alveolar hemorrhage syndromes?
    • Primary immune mediated diseases
    • Goodpasture syndrome
    • Wegener's granulomatosis
    • Idiopathic pulmonary hemosiderosis.
  10. What causes Goodpasture syndrome?
    Antibodies to the non-collagenous domain of the alpha-3 chain of collagen 4.
  11. What is characteristically seen after an acute presentation of goodpasture syndrome?
    Hemosiderin, either within macrophages or extracellularly.
  12. Wegener's granulomatosis (WG) is also known as?
    Pulmonary angiitis and granulomatosis.
  13. 90% of patients with WG test positive for?
    c-ANCA.
  14. What are some manifestations of WG?
    • Upper respiratory: epistaxis, chronic sinusitis, nasal perforation
    • Pulmonary: cough, hemoptysis, chest pain.
  15. Lung lesions in WG are characterized by?
    • Necrotizing vasculitis (angiitis)
    • parenchymal necrotizing granulomatous inflammation.
  16. Acute bacterial pneumonias can present as?
    • Bronchopneumonia: patchy distribution of inflammation with infection of bronchi, bronchioles and adjacent alveoli (usually involving more than one lobe)
    • Lobar pneumonia: contiguous airspaces of part of all of a lobe homogenously filled with exudate.
  17. What is the most common cause of (community-acquired) pneumonia?
    Streptococcus pneumoniae (pneumococcus).
  18. What are the four stages of pneumonia (gross and histology)?
    • Congestion: Lung is heavy and red
    • Red hepatization: Exudate with red cells, fibrin, and neutrophils fills alveoli
    • Gray hepatization: Disintegration of red cells but persistence of fibrinopurulent exudate
    • Resolution: enzymatic digestion of exudate.
  19. What is the most common cause of acute exacerbation of COPD?
    Haemophilus influenzae.
  20. What is the most frequent cause of gram negative pneumonia?
    • Klebsiella pneumoniae
    • Seen in chronic alcoholics
    • Thick and gelatinous sputum.
  21. what is the histologic presentation of mycoplasma pneumoniae?
    • children and young adults
    • inflammation reaction confined to the interstituim (exudate-free alveolar spaces).
  22. What caused SARS (severe acute respiratory syndrome)?
    A novel coronavirus (single stranded RNA).
  23. What is the Ghon complex?
    • Initial focus of primary TB infection
    • Includes the parenchymal subpleural lesion and the caseous lymph nodes draining the focus
    • Necrotizing, caseating granulomas.
  24. How do you diagnose TB?
    Demonstration of acid-fast organism in sputum culture.
  25. What does mucormycosis look like histologically?
    Non-septated hyphae with irregular branching.
  26. What does aspergillosis look like histologically?
    Septated hyphae with 45 degree branching.
  27. Cryptococcosis usually presents in which patients?
    • Opportunisitic infection in immunocompromised hosts
    • pulmonary, CNS, or disseminated disease.
  28. Name another opportunistic infectious fungus?
    • Pneumocystis jiroveci
    • intra-alveolar, foamy exudate
    • cup-shaped cyst walls on silver stain.
  29. What is the most common cause of peripheral arterial disease (PAD)?
    Atherosclerosis.
  30. What is the most important modifiable risk factor for developing PAD?
    • Smoking
    • Diabetes is the other risk factor.
  31. What are five pathologies of PAD?
    • Obstructive
    • Embolic
    • Aneurysm
    • Pseudoaneurysm
    • arterio-venous shunt.
  32. What are three different clinical syndromes caused by PAD?
    • Intermittent claudication (IC): most common symptom, relieved at rest
    • Critical limb ischemia (CLI)
    • Acute limb ischemia (ALI).
  33. What are the most common sites of PAD causing IC?
    • Femoral and popliteal arteries (lower limb)
    • Brachiocephalic and subclavian can cause arm claudication (much less common).

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