Slide 1

Haemodynamics The principles of blood flow are called haemodynamics

Hyperemia and congestion are the terms used for localised increase inthe volume of blood within the dilated vessels of an organ/tissue

Hyperemia CongestionEg: At sites of inflammation2. In skeletal muscle during exercise3. Blushing flushing of skin of face in response to emotions4. Menopausal flush Increased blood flowEg: 1. systemic in cardiac failure2. Isolated in venous obstruction3. Reduced outflow of blood from a tissue

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 tissuesEffusion: When the serosal surface is involved, fluid may accumalate in the adjacent body cavity as an effusion

Left sided heart failureEtiology Systemic hypertension most common causeIschemic heart diseaseAortic or mitral valve diseasePrimary myocardial disease

Clinical presentations of LHFObstruction 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 necrosis3. Reduced CNS perfusion causes hypoxic encephalopathy ( irritation to coma)

Clinical presentation of RHFCongestion and edema of portal and dependent peripheral areaEg: feet, ankle and sacrum, effusions in pleura and peritoneumCVC spleenCVC LiverAcute tubular necrosis

CVC LiverEtiology- Right heart failureOcclusion of inferior vena cava and hepatic veinGross Liver enlarged and tender Capsule tense C/S nutmeg appearanceCentral 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)

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

CVC LungEtiology left heart failure in rheumatic mitral stenosisGross 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

Histology: Acute pulmonary congestionAlveolar septa widened( due to dilated and congested capillaries)Focal intra-alveolar hemorrhage Alveolar septal edemaChronic pulmonary congestionAlveolar septa thickened increased fibrous tissue rupture of dilated and congested capillariesleads to hemosiderin laden macrophages inalveoli called as heart failure cells

CVC SpleenEtiology Right heart failure Portal hypertension from cirrhosis of liverGross Spleen enlargedOrgan congested, tense and cyanoticC/S grey tan

Microscopy: Red pulp enlargedCongestion and marked sinusoidal dilatationFoci of recent and old hemorrhagesHyperplasia of reticuloendothelial cells in red pulpFibrous thickening of capsule and trabeculaeGamma-gandy bodies / haemosiderofibrotic nodulesAdvanced stage firm spleen hepatic cirrhosis (congestive splenomegaly)

CVC KidneyGross - Kidney enlarged Medulla congestedMicroscopy Degenerative changes in tubulesCloudy swelling, fatty change

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

2. Sectioned surface of lung shows brown induration in:Pulmonary embolismPulmonary haemorrhagePulmonary infarctionCVC Lung

MCQ1. Transudate differs from exudate in having the following except:No inflammatory cellsLow glucose contentLow protein contentLow specific gravity

2. The following type of edema is characteristically dependent edema:Nephrotic oedemaNephritic oedemaPulmonary oedemaCardiac oedema

3. Pulmonary oedema appears due to elevated pulmonary hydrostatic pressure when the fluid accumalation is:Two foldFour foldEight foldTen fold

Key for MCQBDDBD

2nd Year Pathology 2010OedemaExtravascular 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 spaceEffusion = increased fluid in a body cavityOedema and effusions have similar pathogenesis

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

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 lymphaticsNo net increase in interstitial fluid volume

2nd Year Pathology 2010Normal homeostasisARTERIOLEVENULECAPILLARY BED

Net flow inNo net flowNet flow out

LYMPHATICSExcess fluid

hydrostatic Poncotic P

2nd Year Pathology 2010Increased hydrostatic pressureARTERIOLEVENULECAPILLARY BED

No net flowNet flow out

hydrostatic Poncotic P

Net flow outOverall excess flow out

2nd Year Pathology 2010Decreased oncotic pressureARTERIOLEVENULECAPILLARY BED

No net flowNet flow out

hydrostatic Poncotic P

Net flow outOverall excess flow out

2nd Year Pathology 2010Lymphatic obstructionARTERIOLEVENULECAPILLARY BED

Net flow inNo net flowNet flow out

Excess fluid

hydrostatic Poncotic P

Excess fluid collectsLYMPHATIC

2nd Year Pathology 2010Pathogenesis of OedemaIncreased hydrostatic pressureReduced plasma oncotic pressureLymphatic obstructionSodium and water retention

Inflammation

Protein-poor transudateProtein-rich exudate

Increased hydrostatic pressure Results in increased outflow of fluid

Causes: Impaired venous returnCongestive heart failure / constrictive pericarditis Arteriolar dilatation - heat / neurohumoral dysregulation

2nd Year Pathology 2010Results in decreased resorption of fluidCauses:nephrotic syndromecirrhosisprotein losing enteropathiesmalnutritionReduced oncotic pressure

2nd Year Pathology 2010Lymphatic obstructionResults in decreased resorption of fluidUsually localisedCauses:Surgical removal of lymph nodes and lymphaticsTumour metastases to lymph nodesIrradiationFilariasis (parasitic infection)

2nd Year Pathology 2010Sodium and water retentionResults in: Expansion of intravascular fluid volumeIncreased hydrostatic pressureDilutional decrease in vascular osmotic pressure

2nd Year Pathology 2010Sodium and water retentionCauses:Excessive salt intakeRenal 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

2nd Year Pathology 2010 Inflammation

Due to vasodilation and hyperpermeable vesselsvasoactive mediators e.g. Histamine, cytokines e.g. IL-1, TNF

Characterised by: protein-rich and inflammatory cell-rich exudateUsually localized to sites of acute inflammationCan be generalised and life-threatening e.g. anaphylaxis

2nd Year Pathology 2010

Localised oedema - blisterGeneralised oedema laryngeal oedema in anaphylaxis

2nd Year Pathology 2010Pitting Subcutaneous Oedema

2nd Year Pathology 2010Cerebral Oedema & HerniationFlattened sulci and uncal herniation

2nd Year Pathology 2010Cerebral Oedema & Herniation

Tonsillar herniation and pontine haemorrhage

2nd Year Pathology 2010EffusionsSimilar pathogenesis and aetiology as oedemaIncreased hydrostatic pressureLeft heart failure: HypoproteinaemiaCirrhosis - ascitesFluid overload (salt and water retention)Renal failureInflammationPleural effusion associated with pneumonia / TB

Grossly 1. organomegaly or tissue swelling2. subcutaneous tissues /dependent body parts: sacrum / legs, pitting oedema 3. Tissues with loose extracellular matrix (ECM): eyelids4. Lungs - heavy, contain frothy blood-tinged fluid5. Brain swollen with narrowed sulci and flattened gyri , +/- evidence of herniation

2nd Year Pathology 2010Serous pleural effusion

2nd Year Pathology 2010Serosanginous pleural effusion

2nd Year Pathology 2010Fibrinous pericarditis

2nd Year Pathology 2010Chylous Ascites

2nd Year Pathology 2010Acute pulmonary oedema

2nd Year Pathology 2010EffusionsTransudates:Serous: mainly edema fluid, very few cellspleural effusion = hydrothoraxpericardial effusion = hydropericardiumperitoneal effusion = hydroperitoneum / ascitesExudate : Fibrinous (serofibrinous): protein-rich exudate containing fibrin strandsPurulent: numerous inflammatory cells, mainly neutrophils(also called "empyema" in the pleural space)

2nd Year Pathology 2010Haemorrhagic (blood): hemo-thorax/pericardium/peritoneumCause: trauma, ruptured MI / aortic aneurysm

Chylous (lymphatic fluid): chylo-thorax/pericardium/peritoneumCause: trauma (often surgical) to major lymphatic vessels