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Respiratory Path III

Respiratory Path III. Vascular and Hemodynamic Pathology. Topics Covered In This Lecture. 1 .Pulmonary Edema. 2.Acute respiratory distress syndrome (ARDS). 3.SARS (Severe acute respiratory syndrome). 4.Pulmonary Embolism. 5.Pulmonary Hypertension. 49. Alveolar wall microscopy.

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Respiratory Path III

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  1. Respiratory Path III Vascular and Hemodynamic Pathology

  2. Topics Covered In ThisLecture 1.Pulmonary Edema 2.Acute respiratory distresssyndrome (ARDS) 3.SARS (Severe acuterespiratory syndrome) 4.Pulmonary Embolism 5.Pulmonary Hypertension 49

  3. Alveolar wall microscopy

  4. Case History • 72 yr old extremely pleasant Caucasian male with a past medicalhistory of CABG and multiple stents,unstable angina and myelodysplasticsyndrome, presented with left armpain • He was admitted, but died within 24hours • A post mortem was performed. 50 S.

  5. Post mortem findings • Right lung weighed 1,100 g and theleft lung weighed 750 g • Severe coronary atherosclerosis wasnoted • There was evidence of acute myocardial infarction and massivepulmonary edema 51

  6. Causes of PulmonaryEdema • Hemodynamic disturbances - Increased hydrostatic pressure • Left sided congestive heart failure – Heavy wet lungs (basal regions of lower lobes) - Alveolar capillaries engorged - Intra-alveolar granular pink precipitate - Heart failure cells; brown discoloration - Impairs pulmonary function and predisposesto infection 52 S.

  7. Pulmonary Edema- Causes Hemodynamic Increased hydrostatic pressure • Left ventricular failure (common) • Excess IV fluids,Excess blood transfusion. Decreased oncotic pressure • Severe hypoproteinemia, Liver disease,Nephrotic syndrome Other • Lymphatic obstruction (carcinoma, rare) 53 S.

  8. Pulmonary edema--Causes Microvascular Injury • Damage to vascular endothelium •Leekage of fluid and proteins intointerstitium and lumen • Diffuse edema is a contributor to acute respiratory distress syndrome 54 S.

  9. Microvascular injury • Infections: Pneumonia, septicemia • Inhaled gases: Oxygen, smoke • Liquid aspiration: Gastric contents • Drugs and chemicals:Chemotherapyagents, heroin, cocaine, paraquatpoisoning • Shock, trauma • Radiation • Transfusion related 55 S.

  10. Adult(Acute) RespiratoryDistress Syndrome (ARDS) Syn. Shock Lung Syndrome, Diffusealveolar damage (DAD), Acute lunginjury (ALI) (cf. RDS in neonates due todeficiency of surfactant) Clinical syndrome caused by diffusealveolar damage 56 S.

  11. Mechanism of ARDS • Imbalance between pro-inflammatoryand anti inflammatory cytokines • Toll like receptors activate NF-kB, atranscription factor controllingexpression of pro-inflammatorygenes • IL-10 is anti-inflammatory cytokine • Modification of the transcription cascade may be a logical future S. 57 target for ALI n-

  12. ALI, Early ARDS

  13. ARDS Endotheliumnecrosis Type I alveolarcells necrosis Fibrin Edema Waxy Hyalinemembranes 59 S.

  14. Diffuse Alveolar Injury

  15. Shock lung • Endothelial damage, damage to type 1pneumocytes •Exudate, impaired gas exchange •Hyaline membrane (necrotic debris from epithelial cells plus edema fluid coagulate) • Type II pneumonocyte necrosis- loss of surfactant- microatelectasis 60 S.

  16. What Causes ARDS? • Infections* • Sepsis* • Head injuries* • Gastric aspiration* • Pancreatitis • Burns • Trauma • Fractures with fat embolism Infection,sepsis,head injuries and gastric aspiration Account for more than 50 %of cases. 61 S.

  17. Clinical features • Serious disorder • Respiratory difficulty- acute • Gasping for breath • Severe hypoxemia, cyanosis, unresponsive to oxygen • Bilateral infiltrates on chest X-ray •Absence of clinical features of LVF • High mortality: 40% in 190,000 ARDS cases/yr • Patchy distribution • Healing may result in diffuse interstitial fibrosis 62 S.

  18. Phases of ARDS • Exudation- 0-7 days • Proliferation - 1-3 weeks macrophages phagocytose deadcells and hyaline membrane, typeII pneumonocytes proliferatemature in to type I cells • Fibrosis- TGF-β, PDGF 63 S.

  19. SARS (Severe acute respiratory syndrome) • First appeared in China in Nov 2002; last case 2004 •Cause -- Corona virus; 8000 cases; 774 deaths • 2-10 day incubation period;begins with dry cough, malaise, myalgia, fever, chills • 1/3rd fight infection, but 2/3rd progress to severe respiratory disease, shortness of breath, tachypnea,and pleurisy • 10% of patients die from illness • First transmitted through wild masked palm civets •Patho-physiology unknown; how virus moved from animals to humans unknown 64 S.

  20. Wild masked palm civet

  21. Pulmonary embolismPulmonary Infarction • Causes more than 50,000 US deaths/year • Large pulmonary embolus is a causesudden instantaneous death • Blood clots that occlude large pulmonaryvessels are embolic •Usual source of pulmonary emboli are thedeep veins of the leg 65 S.

  22. Pulmonary embolism • 95% from deep leg veins • Sick, bedridden patients with pulmonary, cardiovascular disease • BIG embolus -> bifurcation of PA, sudden death from acute right heart failure - no time to develop any changes in lungs 66 S.

  23. Pulmonary embolism • MEDIUM -> hemorrhage, infarction only if circulatory status alreadycompromized • SMALL -> usually no infarct because of dual supply, resolve ( lysis), - if recurrent- pulmonary hypertension 67 S.

  24. Saddle embolism

  25. Infarction • Clinically resembles myocardial infarction - chest pain, dyspnea,shock • Gross: Wedge shaped, hemorrhagic infarct, may be multiple • Micro: coagulation necrosis 68 S.

  26. Pulmonary Infarction

  27. Pulmonary hypertension • When pulmonary pressure reaches 1/4thof systemic levels • Primary PH - BMPR2 locus mutations • Rare, young women,recurrentdyspnea ,syncope •Raynaud’s phenomenon (vasopasm of peripheral vessels) • ? Neurohormonal hyperactivity • ? Vasotropic virus- HSV 8 73 S.

  28. BMPR2 • bone morphogenetic protein receptor, type 2 (BMPR2) • a cell surface molecule that binds to a variety of TGF-β pathway ligands • It is normaly inhibitory to vacular proliferation. • Hence Loss of function mutation affecting the gene would lead to excessive vascular proliferation. • Implicated in 50 % of cases of Primary pulmonary hypertension.

  29. Pulmonary hypertension • Secondary PH • COPD - Chronic bronchitis, emphysema, diffuse fibrosis • Congenital L-R shunts- VSD • Recurrent pulmonary thromboembolism in small sizedvessels 74 S.

  30. Pulmonary hypertension Mild - Elastic duplication Normal pulmonaryartery Medial hypertrophy,Intimal fibrosis Severe,plexiform lesions - 75

  31. Pulmonary hypertension 76 S.

  32. Morphology of pulmonary hypertension • Changes in medium sized arteries • Medial thickening •Intimal hyperplasia / fibrosis • Reduplication of elastic layer 78 S.

  33. Morphology of pulmonary hypertension •Plexiform changes in severe varieties only (primary) • Necrosis of wall (fibrinoid) • Thrombosis • Rupture, bleed • Dilation lesions, angiomatoid lesions •Hemosiderin 79 S.

  34. Plexiform Lesions. • Plexiform lesions are found : • Primary pulmonary hypertension, • Certain congenital heart disease. • Pulmonary hypertension of AIDS, • Schistosomiasis, • Cirrhosis of the liver, • Ingestion of certain diet pills,

  35. Plexiform lesions

  36. Primary pulmonary hypertension- clinical • Symptoms appear late • Fatigue, dyspnoea • Syncope on exercise • Chest pain • Respiratory insufficiency, cyanosis •Corpulmonale 80 S.

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