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*Haemodynamic disturbances *Venous congestion *Oedema *Bleeding *Pathological thrombosis *Embolism *Ischemia & Infarction *Shock Venous congestion :accumulation of blood in the venous site of the circulation due to obstruction of the venous return. It cause bluish discoloration of skin due to accumulation of stagnated blood contianing deoxygenated hemoglobin and it should be differentiate from other term which is hyperaemia which is also increase in the amount of blood in the artierioles of the affected tissue or organ but it is an active process due to neurogenic mechanism cause arteriolar dilitation and local redness due to accumulation of oxygenated blood e.g acute inflammation. I-systemic venous congestion: Here the systemic vein is congested and it is usually seen in right side heart failure which is due to 1 pulmonary valve stenosis or due to diseases of the lung. Chronic venous congestion lead to hypoxia which cause degeneration & necrosis . its effect mainly seen in the abdominal viscera such as liver .spleen and kidney. Structural changes of systemic venous congestion : In addition to generalized oedema , structural changes are seen in liver ,spleen and kidney. In liver grossly it is enlarge ,firm , cut surface show mottled or nutmeg appearance . Mic :. *The central vein & the surrounding sinusiod are distended with blood (red ) * The surrounding hepatocyte show fatty changes( pale) . . * The dark central area surrounded by paler area producing nut meg liver. * With time chronic congestion lead to fibrosis in the centrilobular area associated with hyperplastic nodule resulting from compensatory proliferation of the surrounding paranchyma producing cardiac cirrhosis. 2 Spleen become enlarge and firm grossly. Microscopically Congestion of the sinusoid of the red pulp which appear black while the white pulp appear as pale spot. 2- Pulmonary venous congestion: Seen in left sided heart failure (due to systemic hypertention,coronary heart disease ) which lead to increase pressure in the left atrium and pulmonary vein .. Microscopically: Congestion of the venules and alveolar capillary . alveolar space filled with RBCs & heamosidrin laden macrophage(heart failure cell) . the heamosidrin causing irritation and subsequent fibrosis of the alveolar wall. 3 The condition is called brown induration of the lung due to associated fibrosis with brown color of heamosidrin . 3-Local venous congestion:. Due to mechanical interference with the venous drainage from an organ or limb could be : 1-acute due to ligation or thrombosis of the blood vessel . 2-chronic as in fibrosis of b.v wall , pressure from outside by tumor or organized thrombosis . Oedema: Oedema is an abnormal accumulation of fluid in the interstitial space and it is either generalize or localize. Oedematous fluid is either of transudate or exudate. The transudes (non inflammatoryoedema) usually contain few cells , with low protien <3gm/dl and low specific gravity less than 1.010 , in contrast to the exudates(inflammatory oedema) in which the cells are numerous , protein is more than 3 gm/dl & specific gravity is more than 1.010 4 Causes ,pathogenesis of non inflammatory oedema : 1- Increase in the hydrostatic pressure : as in right sided heart failure . 2- decrease in the colloid ( oncotic ) pressure : due to reduction in albumin synthesis or increase in protein loss as in nephrotic syndrome . 3- Lymphatic obstruction : usually localize due to inflammation or obstruction by tumour . 4- Sodium & water retention due to impairment in renal function , both can cause increase in the hydrostatic pressure & diminish in the oncotic pressure . A : Generalized oedema Causes(types): 1- cardiac oedema: due to sever heart failure : A: there is reduction in cardiac out put→↓ in renal flow and glomular filterate rate , so this will stimulate the secretion of renin which stimulate the secretion of aldosteron causing retention of Na & water retention . B:Could be due to accumulation of waste product in the interstitial tissue which will rise the osmotic pressure there so more water is withdrawn from circulation .. 5 C:Chronic hypoxia →↑vascular permeability so more water and Na will pass outside b.v. D: Reduction in venous return → increase in the hydrostatic pressure at the venous end so cause reduction in the re-entry of fluid to the circulate. 2- Renal oedema: could be due to : A-Nephrotic syndrome which is a group of disease characterized by heavy proteinuria →hydpoproteinemia that cause generalize oedema. B- it could be due to disease affect glomeruli as in acute diffuse glomerularnephritis which have reduction in renal blood flow and decrease glomerular filtration rate the cause of which is unknown and may be due to defect in rennin angiotension system. 3- Nutritional oedema: it is seen in sever malnutrition as in kwashiorkor which could be due to low plasma protein or due to replacement of subcutaneous fat by loose C.T causing low tissue tension and enhance the accumulation of fluid. 6 4-Hepatic oedema : the cause is not well known could be due to hypoproteinemia. B: Localized oedema: 1-Acute inflammation : due to increase in hydrostatic pressure which enhance exudation of fluid , due to increase in vascular permeability so protien escape outside bv so oncotic pressure is reduced and this enhance the accumulation of blood outside the b.v 2- Local venous obstruction : physiological as in oedema of the leg follow prolong sitting without leg movement OR pathological due to deep vein thrombosis of the leg . 3- chronic lymphatic obstruction: as in tumor press or invade lymphatic wall or due to chronic inflammation of lymphatic vessel . 4-Pulmonary oedema: cause : A-due to increase in hydrostatic pressure of pulmonary circulation as in left ventricular failure. 7 B-overloading of circulation as in rapid blood transfusion in anemic patient. C-asapart of generalize oedema as in glomerulonephritis. D- increase in intracranial pressure as in head injury . Heamorrhage: Extravasations of blood due to rupture of b.v or due to group of clinical disorder called heamorrhage diathesis( bleeding tendency ) . Types of bleeding : *-bleeding either external . *-or internal : -- hematoma : accumulation of blood in the tissue . -- Peticheal hemorrhage : minute bleeding (12mm) (due to reduction in platelets number or , platelet dysfunction ). 8 -- purpura : bleeding (3-5 mm) in the skin , its causes as above or due to vasculitis). -- ecchymosis : (1-2cm) bleeding in the skin which has early red blue color due to accumulation of (Hb) →blue green (bilirubin)→golden yellow (heamosidrin). -- large bleeding may accumulate into body cavity forming heamoperitonium, haemothorax haemopericardium. Effect of bleeding : depend on : * amount of bleeding . 1- repeated loss of small amount cause iron deficiency anaemia . 2-rapaid loss of 1/3 or more of blood volume cause hypovolemic shock. 3- loss of moderate amount ( about 20% ) is liable for life in healthy person . * Site: small amount of bleeding which has no effect if occur in 9 subcutaneous tissue may cause death if occur in the brain . Pathological thrombosis: Formation of solid or semisolid mass from blood constituent within vascular system during life. The main constituent of thrombi: fibrin ,RBC, WBC & platelet. Composition (types ) of thrombi determine by the rate of blood flow : 1- Pale thrombi: it is seen in artery because of rapid blood flow, it is firm, pale . Mic : compose of platelet mainly with fibrin & some RBC. 10 2-Red thrombi: seen in stagnated blood adjacent to complete occluded blood vessel ,it is soft ,red . Mic : compose of fibrin strand with large no. Of RBC in between with little platelet &WBC. 3- Mixed thrombi: seen in slow blood vessel as in vein. Causes ;( predisposing factor; pathogenesis of thrombosis) : 1-Endothelial injury : seen in ulcerated athermanous plague, abnormal valve of the heart , hypertension & arterities . here platelets adhere to damage surface , release thromboplastin & activate coagulation cascade to produce thrombosis . 2- Change in blood constituent causing hyper viscosity state, this is seen in oral contraceptive ,during pregnancy ,extensive burn , metastatic tumours, , advance age (cause platelet aggregation), smoking, or due to mutation of prothrombin gene . 3-Altration of blood flow either due to turbulence as in atheroma Or due to slowness of blood flow seen in aneurysm , non contracted myocardium as in M.I , hyperviscocity syndrome as in polycythaemia, sickle cell anaemia that cause vascular obstruction& stasis. 11 Morphology of thrombosis : thrombus occur anywhere in cardiovascular system , they are variable in size & shape depend on the site of origin & the condition predispose to its formation . Arterial or cardiac thrombus usually begin at site of endothelial injury or turbulence while venous thrombi occur at site of stasis . All thrombi are firmly attach to the point of origin , arterial thrombi grow in retrograde direction from the point of attachment while venous one extend in the direction of blood flow to the heart. Aortic & cardiac thrombi (mural thrombi ): have laminated appearance called line of zahn produced by pale layer of platelets & fibrin that alternate with darker layer containing more RBC .while in venous thrombi the lines are less apparent & instead it look like blood clot in a test tube . 12 Cardiac thrombus is due to abnormal myocardial contraction ( as myocardial infarction , arrhythmia , cardiomyopathy ) OR due to injury of myocardial surface as in myocarditis .while aortic thrombi is due to ulcerated atheromatous plaque or aneurysmal dilation . Arterial thrombosis are usually occlusive occur in coronary, cerebral & femoral arteries & seen in atheromatous plaque or due to endothelial cell injury as vasculitis or trauma . Venous thrombus (phlebothrombosis) almost occlusive , it create a long cast of the vein lumen & since it associated with stasis it contain more RBC & called red thrombus , usually occur in the lower extremities . red (venous)thrombus clot *dry,friable& firm. rubbery. * adherent to b.v wall . post mortem - gelatinous soft , - not adherent. 13 * show vaque strand . yellow chicken fat over red jelly of pale fibrin . -surface show Thrombosis over heart valve is called vegetation which may occur on damage valve due to infection ( as infective endocarditis) or due to hypercoagulable state (nonbacterial thrombotic endocarditis ) & less commonly occur in association with SLE . Clinical correlation : Thrombus is significant due to obstruction of b.v or due to formation of emboli . Arterial thrombi can embolize but its role in obstruction of cerebral &coronary b.v is much important. while venous thrombi can cause obstruction with distal stasis but its role in embolism is more important .venous thrombosis usually occur in superficial & deep vein of the leg . Superficial vein thrombosis occur in the saphenous vein causing congestion , pain , swelling & tenderness along the vein & may lead to skin infection & varicose ulcer , while embolization is rare . 14 while deep thrombosis (DVT)occur in a deep vein & it is more serious due to embolization & obstruction occur early but later disappear once collateral circulation develop . DVT occur due to: 1- stasis & hypercogulable state as in heart failure . 2-Reduce physical activity as advance age with bed rest .burn ,trauma & surgery due to reduce milking action of muscle of the legs. 3- Pregnancy & post partum period due to infusion of amniotic fluid or hypercoagulability . . 4 which -Disseminated tumour as in carcinoma of head of pancrease have a high risk of thrombotic phenomena. Fate of thrombosis(result): 1-If small undergo lyses i.e. digestion by plasmin or proteolytic enzyme of neutrophilis. 2-In occluding thrombi which contain a lot of clot , retraction of the clot may occur so new canal will form 15 which is lined by endothelial cell result in recanalization. 3-Organisation & recanalization : this is seen in arterial thrombi in which we have invasion & digestion by macrophage following by in growth of fibrovascular granulation tissue. 4-Calcification in the form of dystrophic calcification 5-Part of it detached →embolism. 6-Infection of thrombi so it is become friable & part of it detached → pyaemic abscess or septic infarction . Embolism : An emboli is an abnormal ,undissolved mass carried by blood stream with subsequent impaction in another vessel any where in the body & the process is termed embolism. Types : 1-thrombotic emboli which is the commonest (95%) & can be carried by arteries & veins . *Systemic( Arterial emboli) usually arise from : a- mural thrombi in the left ventricle following M.I .16 b- less commonly they may arise from left atrium as in fibrillation. c -aortic athermanous plague . d- vegetation on diseased value . They can lodge any where in the arterial system & invariably cause Infarction Usually in the lower extremity , brain , kidney & spleen. *-Venous emboli (pulmonary embolism ), they usually originate from deep vein thrombosis ( D.V.T ) of the leg , it then pass to the right side of the heart & then to the lung: --Majority are asymptomatic . -- large emboli can settle at the pulmonary artery bifurcation or large artery & may cause death or right side heart failure . --smaller emboli will produce pulmonary infarction or pulmonary hemorrhage . -- very rare venous emboli may pass to the systemic circulation through a defect in the heart septum & called paradoxical embolism. 2-Fat embolism :characterized by progressive dyspnoea ,convulsion & sometime renal failure develop 24-72 hrs after sever compression to the 17 adipose tissue or bone fracture, here fat droplet enter ruptured blood vessel at the site of trauma & deposited at the cerebral ,pulmonary & renal vasculature cause occlusion. 3-Air embolism : can occur when air enter large vein following lung, chest or neck injury . smaller quantities usually dissolve in the plasma. Caisson disease occur when deep sea diver is brought up rapidly to the atmospheric pressure so nitrogen gas which was dissolve under high pressure is released in the plasma form numerous small gas bubbles which obstruct blood vessel throughout the body produce characteristic joint & muscle pain . 4-Amniotic fluid embolism :occur in prolong or traumatic labour . 5-Malignant tumor emboli : causing secondary metastasis . 6-Parasitic emboli. Ischemia : It is inadequate blood supply to an area of a tissue. Causes of ischemia : 18 1- 99% it result from thrombotic or embolic mechanism . 2- complicated atheroma . i.e. atheroma with subsequent hemorrhage. 3-twisting of blood vessel. 4-compression from out side by tumor or by entrapment in a hernial sac. 5- venous obstruction can occur in a varicose vein. Effect of ischemia: Variable depend on the adequacy of collateral circulation , if a good collateral is present it will produce little or no effect but if the collateral circulation is poor, it will lead to functional disturbances or even cell death. Ischemia in the heart can lead to chest pain (angina) , while in lower limb ,it produce intermittent claudication (pain in the calf muscle during exercise ) . Infarction : An area of ischemic necrosis caused by occlusion of arterial supply or venous drainage in a particular tissue . Causes: same as ischemia. 19 Types : (morphologic appearance) It is either red or pale. Red infarction usually follow venous occlusion : * in loose tissue such as lung that allow blood to collect in infarcted area . * in tissue with dual circulation such as lung , intestine . * when flow is re-established to a site of previous arterial occlusion & ischemia e.g fragmentation of occlusive emboli. The color reflect the amount of blood which accumulate in the parenchyma during necrosis. pale infarction occur due to arterial occlusion in solid organ (heart ,spleen .kidney) &the solidity of the organ limit the amount of hemorrhage. Septic infarction : occur when bacterial vegetation from heart valve embolize , or when microbes infect area of necrotic tissue . here infarction convert to an abscess. Grossly : Infarction has a wedge shape , the apex at the site of occluded blood vessels & the periphery of the organ forming the base which is poorly define . 20 With time the edge become more defined by a narrow zone of hyperemia due to inflammation & pale infarction become more paler & sharply defined while red infarction it become more firm & brown. Microscopic feature: * the histological features is that of coagulative necrosis with the exception of the brain which show liquefactive necrosis .these changes seen 12 hr- 18hr after the onset . * within 1-2 days evidence of acute inflammation become prominent. *this is followed by stage of healing by granulation tissue which end in scar tissue in most of infarction. Susceptibility of tissue to ischemia : (Factors that influence the development of infarction) : The consequence of vascular occlusion can range from no or little effect, to death of tissue or even the individual. In general the extent of infarction is usually less than that of tissue supplied by that occluded artery . it depend on: 1- nature of vascular supply. The size of infarction depend on whether the collateral circulation are healthy and capable of dilation.. 21 So tissue which has duel blood supply as the lung or intestine are relatively resistant to necrosis. 2- The capability of tissue to withstand ischemia: neuron suffer from infarction if blood supply is deprived for 3 minutes while cardiac muscle can withstand hypoxia up to 20-30 minute in contrast to fibrous , fatty and bone tissue which are less susceptible to ischemia. 3- Rate of development of occlusion: slowly developing occlusion are less liable to cause infarction. 4-Oxygen content of blood: partial occlusion of small vessel in anemia or cyanotic patient may lead to infarction Shock: heamodynemia change result from inadequate tissue perfusion due to acute fall in cardiac output . At the beginning these changes are helpful in maintaining the blood supply to the vital organ such as (heart and brain) by reducing the blood supply to other tissue of the body. However if the Cardiac output is not corrected it will cause damage to the cells of vital tissue lead to multiple organ failure. Types of shock and causes: 22 1- Cardiogenic shock: it is due to acute cardiac insufficiency as in M.I., sever myocarditis, cardiac surgery. 2- Hypovolaemic shock: it is due to reduce in blood volume as in sever bleeding, extensive vascular exudation as in burn and condition which cause dehydration. If the blood loss is up to 10% it has no effect . If the blood loss reach 20% lead to significant hypovolaemia . If the blood exceed 50% lead to death unless urgent treatment is given. 3- Septic shock: usually followed sever infection with septicemia caused by gram negative bacilli which form endotoxin; as in sever burn, generalize peritonitis, surgical operation and instrumentation of urogenital tract. The patient has generalize features of shock in addition to fever. 4- Neurogenic shock ;due to anesthetic accident or spinal cord accident. 5- Anaphylactic shock: cause by generalize IgE hypersensitivity reaction forming systemic vasodilation & increase vascular permeability. 23 Stages (pathogenesis) of shock and hypovoleamic shock: 1-An initial compensatory stage during which reflex compensatory mechanisms occurred to maintain C.O.P. result in tachycardia, peripheral vasoconstriction and renal preservation of fluid. So cardiac output is improved and perfusion of vital organ is maintain . 2-A progressive stage occur if the underlying cause is not correct characterized by tissue hypo perfusion & hypoxia which stimulate anaerobic glycolysis with execs lactic acid production lead to lower PH of the tissue with subsequent vasodilatation and pooling of blood in the microcirculation lead to decrease C.O.P. 3-Irreversible stage occur if early treatment isn’t take place and death occur even if heamodynamic defect is corrected. Clinical feature: Pale, cold, sweaty skin and even cyanosis; rapid weak pulse, decrease in blood pressure and increase in rate and depth of respiration. The patient become restless, confuse and may lead to coma. Pathological change of shock: 24 Shock usually affect the function of the cell. However it cause swelling of all cell and some time fatty changes. Different organ involved in shock including: 1- Lung which show oedema congestion, hyaline disease, collapse and bronchopneumonia. 2- Liver may show centrilobular necrosis. 3- Kidney may show acute tubular necrosis. 4- stress ulcer in ulcer in stomach . 5- disseminated intravascular coagulation (DIC). ( which characterize by thrombosis in microcirculation with subsequent hemorrhage). 25