Hyperemia and congestion edema

Hyperemia and congestion edema

1. Haemodynamics The principles of blood flow are called haemodynamics Hyperemia and congestion are the terms used for localised increase in the volume of blood within the dilated vessels of an organ/tissue

2. Hyperemia Congestion Eg : At sites of inflammation 2. In skeletal muscle during exercise 3. Blushing – flushing of skin of face in response to emotions 4. Menopausal flush Increased blood flow Eg : 1. systemic in cardiac failure 2. Isolated in venous obstruction 3. Reduced outflow of blood from a tissue

3. Hyperemia and congestion Hydrostatic pressure is increased in both the conditions, hence, hyperemia and congestion are always associated with edema Edema: Accumalation of fluid in tissues Effusion: When the serosal surface is involved, fluid may accumalate in the adjacent body cavity as an effusion

4. Left sided heart failure Etiology – Systemic hypertension – most common cause Ischemic heart disease Aortic or mitral valve disease Primary myocardial disease

5. Clinical presentations of LHF Obstruction to pulmonary vascular outflow leads to pulmonary congestion and edema Reduced renal perfusion leads to - salt and water retention - reduced excretion of waste products - azotemia - ischemic tubular necrosis 3. Reduced CNS perfusion causes hypoxic encephalopathy ( irritation to coma)

6. Clinical presentation of RHF Congestion and edema of portal and dependent peripheral area Eg : feet, ankle and sacrum, effusions in pleura and peritoneum CVC spleen CVC Liver Acute tubular necrosis

7. CVC Liver Etiology - Right heart failure Occlusion of inferior vena cava and hepatic vein Gross – Liver enlarged and tender Capsule tense C/S – nutmeg appearance Central regions of hepatic lobules are grossly red-brown and slightly depressed owing to loss of cells and are accentuated against the sorrounding zones of uncongested tan liver (nut meg liver)

8. Microscopy – Congestion more marked in the centrilobular zone due to severe hypoxia than at peripheral zone. So, fatty change in the hepatocytes Centrilobular hemorrhagic necrosis Long cases – fibrosis and regeneration of hepatocytes leading to cardiac cirrhosis

9. CVC Lung Etiology – left heart failure in rheumatic mitral stenosis Gross – Lungs – heavy and firm in consistency C/S – dark, sometimes rusty brown in color referred to as brown induration of lungs brown induration is due to pigmentation and fibrosis

10. Histology: Acute pulmonary congestion Alveolar septa widened ( due to dilated and congested capillaries) Focal intra-alveolar hemorrhage Alveolar septal edema Chronic pulmonary congestion Alveolar septa thickened – increased fibrous tissue rupture of dilated and congested capillaries leads to hemosiderin laden macrophages in alveoli called as heart failure cells

11. CVC Spleen Etiology – Right heart failure Portal hypertension from cirrhosis of liver Gross – Spleen enlarged Organ – congested, tense and cyanotic C/S – grey tan

12. Microscopy: Red pulp – enlarged Congestion and marked sinusoidal dilatation Foci of recent and old hemorrhages Hyperplasia of reticuloendothelial cells in red pulp Fibrous thickening of capsule and trabeculae Gamma- gandy bodies / haemosiderofibrotic nodules Advanced stage – firm spleen hepatic cirrhosis (congestive splenomegaly )

13. CVC Kidney Gross - Kidney enlarged Medulla – congested Microscopy – Degenerative changes in tubules Cloudy swelling, fatty change

14. 1. Active hyperaemia is the result of: A) Dilatation of capillaries B) Dilatation of arterioles C) Venous engorgement D) Lymphatic obstruction

15. 2. Sectioned surface of lung shows brown induration in: Pulmonary embolism Pulmonary haemorrhage Pulmonary infarction CVC Lung

16. MCQ 1 . Transudate differs from exudate in having the following except: No inflammatory cells Low glucose content Low protein content Low specific gravity

17. 2. The following type of edema is characteristically dependent edema: Nephrotic oedema Nephritic oedema Pulmonary oedema Cardiac oedema

18. 3. Pulmonary oedema appears due to elevated pulmonary hydrostatic pressure when the fluid accumalation is: Two fold Four fold Eight fold Ten fold

19. Key for MCQ B D D B D

20. 2nd Year Pathology 2010 Oedema Extravascular fluid collections can be classified as follows: Exudate : rich in protein and/or cells (grossly cloudy) Transudate : an ultrafiltrate of plasma with little protein and few or no cells (grossly clear) Oedema = increased volume of fluid in interstitial space Effusion = increased fluid in a body cavity Oedema and effusions have similar pathogenesis

21. 2nd Year Pathology 2010 Normal homeostasis Movement of fluid between microcirculation (arterioles, capillaries, veins) and interstitium dependent on intravascular hydrostatic pressure intravascular colloid osmotic pressure

22. Normally Net outflow at arteriolar end (hydrostatic > osmotic) No net flow across capillaries (hydrostatic = osmotic) Net inflow at venular end (hydrostatic < osmotic) Any excess interstitial fluid removed by lymphatics No net increase in interstitial fluid volume

23. 2nd Year Pathology 2010 Normal homeostasis ARTERIOLE VENULE CAPILLARY BED Net flow in No net flow Net flow out LYMPHATICS Excess fluid hydrostatic P oncotic P

24. 2nd Year Pathology 2010 Increased hydrostatic pressure ARTERIOLE VENULE CAPILLARY BED No net flow Net flow out hydrostatic P oncotic P Net flow out Overall excess flow out

25. 2nd Year Pathology 2010 Decreased oncotic pressure ARTERIOLE VENULE CAPILLARY BED No net flow Net flow out hydrostatic P oncotic P Net flow out Overall excess flow out

26. 2nd Year Pathology 2010 Lymphatic obstruction ARTERIOLE VENULE CAPILLARY BED Net flow in No net flow Net flow out Excess fluid hydrostatic P oncotic P Excess fluid collects LYMPHATIC

27. 2nd Year Pathology 2010 Pathogenesis of Oedema Increased hydrostatic pressure Reduced plasma oncotic pressure Lymphatic obstruction Sodium and water retention Inflammation Protein-poor transudate Protein-rich exudate

28. Increased hydrostatic pressure Results in increased outflow of fluid Causes : Impaired venous return Congestive heart failure / constrictive pericarditis Arteriolar dilatation - heat / neurohumoral dysregulation

29. 2nd Year Pathology 2010 Results in decreased resorption of fluid Causes: nephrotic syndrome cirrhosis protein losing enteropathies malnutrition Reduced oncotic pressure

30. 2nd Year Pathology 2010 Lymphatic obstruction Results in decreased resorption of fluid Usually localised Causes: Surgical removal of lymph nodes and lymphatics Tumour metastases to lymph nodes Irradiation Filariasis (parasitic infection)

31. 2nd Year Pathology 2010 Sodium and water retention Results in: Expansion of intravascular fluid volume Increased hydrostatic pressure Dilutional decrease in vascular osmotic pressure

32. 2nd Year Pathology 2010 Sodium and water retention Causes: Excessive salt intake Renal diseases - Acute renal failure - Renal hypoperfusion - Chronic renal disease 3. Cardiac failure  Decreased cardiac output  renal hypoperfusion 4 . Hypoproteinaemia  Contraction of blood volume  renal hypoperfusion

33. 2nd Year Pathology 2010 Inflammation Due to vasodilation and hyperpermeable vessels vasoactive mediators e.g. Histamine, cytokines e.g. IL-1, TNF Characterised by: protein-rich and inflammatory cell-rich exudate Usually localized to sites of acute inflammation Can be generalised and life-threatening e.g. anaphylaxis

34. 2nd Year Pathology 2010 Localised oedema - blister Generalised oedema – laryngeal oedema in anaphylaxis

35. 2nd Year Pathology 2010 Pitting Subcutaneous Oedema

36. 2nd Year Pathology 2010 Cerebral Oedema & Herniation Flattened sulci and uncal herniation

37. 2nd Year Pathology 2010 Cerebral Oedema & Herniation Tonsillar herniation and pontine haemorrhage

38. 2nd Year Pathology 2010 Effusions Similar pathogenesis and aetiology as oedema Increased hydrostatic pressure Left heart failure: Hypoproteinaemia Cirrhosis - ascites Fluid overload (salt and water retention) Renal failure Inflammation Pleural effusion associated with pneumonia / TB

39. Grossly 1. organomegaly or tissue swelling 2. subcutaneous tissues /dependent body parts: sacrum / legs, pitting oedema 3. Tissues with loose extracellular matrix (ECM): eyelids 4. Lungs - heavy , contain frothy blood-tinged fluid 5. Brain swollen with narrowed sulci and flattened gyri , +/- evidence of herniation

40. 2nd Year Pathology 2010 Serous pleural effusion

41. 2nd Year Pathology 2010 Serosanginous pleural effusion

42. 2nd Year Pathology 2010 Fibrinous pericarditis

43. 2nd Year Pathology 2010 Chylous Ascites

44. 2nd Year Pathology 2010 Acute pulmonary oedema

45. 2nd Year Pathology 2010 Effusions Transudates : Serous : mainly edema fluid, very few cells pleural effusion = hydrothorax pericardial effusion = hydropericardium peritoneal effusion = hydroperitoneum / ascites Exudate : Fibrinous ( serofibrinous ): protein-rich exudate containing fibrin strands Purulent : numerous inflammatory cells, mainly neutrophils (also called " empyema " in the pleural space)

46. 2nd Year Pathology 2010 Haemorrhagic (blood): hemo -thorax/pericardium/peritoneum Cause: trauma, ruptured MI / aortic aneurysm Chylous (lymphatic fluid): chylo -thorax/pericardium/peritoneum Cause: trauma (often surgical) to major lymphatic vessels