DISORDERS OF VASCULAR FLOW: EDEMA, CONGESTION,
HEMORRHAGE, THROMBOSIS, EMBOLISM.
-survival of cells is dependent on the oxygen provided by normal blood supply disorders of blood supply and exchange of fluid cause most common disorders in medicine:
 -oedema, congestion, haemorrhage, shock,
 -thrombosis, embolism and infarction underlie the most important diseases
 -most common immediate causes of death: myocardial infarction, pulmonary embolism, brain strokes (cerebrovascular accidents)
 EDEMA
Edema- abnormal accumulation of fluid in the intercellular space or in the body cavities
Edema may occur as localized or generalised
Severe and generalised oedema, with marked swelling of the subcutaneous tissue= anasarca oedematous collection in body cavities :
-hydrothorax - chest cavity
-hydropericardium - pericardial cavity
-hydroperitoneum (ascites) - abdominal cavity
 noninflammatory oedema-is called transudate- low amount of proteins pathogenesis of oedema: major factors in pathogenesis of oedema -intravascular hydrostatic pressure and plasma osmotic pressure -have opposing effects
 -Normal state- hydrostatic pressure at the arterial end of capillary is higher than colloid osmotic pressure, on the other hand hydrostatic pressure in venous ends of capillaries is lower, thus fluid leaves at the arterial end and returns at the venous end of capillary, the rest is drained by lymphatics to be returned back to the bloodstream.
Major primary causes of non-inflammatory oedema:
 1.- increased hydrostatic pressure -may results of the impaired venous outflow, caused by thrombosis- most common in legs- thus localized oedema generalised increase in venous pressure- occurs in right-sided congestive heart failure
 2.- reduced osmotic pressure- results from the excessive loss or reduced synthesis of serum albumin
-the most important cause of plasma protein loss- nephrotic syndrome
(increased permeability of glomerular membranes)
-causes of decreased synthesis of plasma proteins- in liver cirrhosis, in severe malnutrition
 3.- lymphatic obstruction - impaired lymphatic drainage results in lymphedema (due to obstruction-inflammatory, neoplastic) filariasis-parasitic infection- often causes massive fibrosis of the lymph nodes and lymphatic channels- excessive lymphedema of legs and external genitalia - elephantiasis cancer of the breast- after dissection of axillary lymph nodes- may cause severe postoperative oedema of the arm
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 4.- sodium retention -water retention in acute reduction of renal function- in acute renal failure
 MORPHOLOGY OF THE EDEMA changes are evident grossly, oedema is encountered most often at three sites
= lower extremities, lungs, brain
 subcutaneous oedema of the lower extremities- manifestation of heart failure (of right ventricle)- legs are subject to the highest hydrostatic pressures.
Distribution of oedema fluid in heart failure is influenced by gravity, it is termed „dependent„. in contrast, oedema in acute renal failure-results of proteinuria and sodium retention, tends to be generalised, more severe than cardiac oedema, affects all parts of the body equally, manifests mostly in loose connective tissue matrices-periorbital oedema
 pulmonary oedema-is a prominent feature of left ventricle heart failure, alveolar spaces are filled with eosinophilic fluid
 oedema of the brain- is encountered in a variety of clinical circumstances, such as brain trauma, meningitis, hypertensive crisis
 HYPEREMIA (CONGESTION)
Congestion-local increase of volume of the blood - caused by dilatation of the small vessels
 active hyperemia:
-results from an augmented arterial inflow
-in muscles during exercise
-in inflammation
 passive hyperemia:
-results from diminished venous outflow, is always accompanied by oedema
-in cardiac failure
-in obstructive venous disease
-chronic passive congestion and oedema of the lungs - indicator of left ventricular cardiac failure
-chronic passive congestion of the liver, kidney, spleen - indicator of right ventricular failure
 HEMORRHAGE
= haemorrhage results from rupture of a blood vessel
-rupture of large artery or vein- caused by some type of injury, such as trauma, atherosclerosis, inflammatory or neoplastic erosion of a blood vessel wall
-rupture of small arteries-in systemic diseases
haemorrhagic diathesis = increased tendency to haemorrhage
Haemorrhages may be -external-may cause exsanguinating
- internal- is referred to if blood is trapped in tissues
 haematoma = general term for haemorrhage hematoma may be even lethal- rupture of abdominal aorta in a dissecting or atherosclerotic aneurysm-massive retroperitoneal hematoma
 petechiae= minor multiple hematomas in the skin, mucosal and serosal surfaces
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 purpura= multiple slightly larger hematomas
 ecchymoses= large subcutaneous or subserous hematomas (more than 1-
2 cm in diameter) blood collection in body cavities:
 hemothorax= the blood accumulates in pleural cavities
 hemopericardium= in pericardial cavity
 hemoperitoneum
 hemarthros
CLINICAL SIGNIFICANCE:
-depends on the volume of blood lost by hemorrhage and on the site of hemorrhage
1.
larger and acute blood loss - may cause posthemorrhagic shock site- when located in brain- even smaller hemorrhage may cause death
2.
repeated external hemorrhages- may result in severe lack of iron- iron deficiency anemia
 THROMBOSIS
Thrombosis- formation of clotted mass of blood, the clotted mass is thrombus thrombus may flow downstream in blood vessel system= embolism the process of clotting and embolism- closely related= thromboembolism potential consequence of embolism and thrombosis= ischemic necrosis= infarction thromboembolic infarctions of heart, brain, lungs, are dominating causes of death
pathogenesis of thrombosis =inappropriate activation of normal hemostasis
Normal hemostasis: three major contributing factors of normal hemostasis- platelets, endothelial cells and coagulation system
-1- intact endothelial cells serve to protect blood platelets and coagulation protein from highly thrombogenic subendothelial substance
(collagen)
-injury to endothelial cells represent a loss of anticoagulative mechanism, contributes to thrombosis
- endothelial injury- the most important influence in thrombogenesis
-thrombi appear often on ulcerated plaques in atherosclerotic arteris
(mostly the aorta), at sites of inflammatory or traumatic injury to arteries
(the walls have been infiltrated by cancer)
-thrombi appear regularly in heart chambers when there has been injury to endocardium (due to hypoxia) adjacent to myocardial infarct or in any form of myocarditis
-2- stasis and turbulence of blood - constitutes the second major thrombogenic influence.
-in normal blood flow- all blood cells are separated from the endothelial surface by a plasma zone devoid of cells-lamelar flow
- stasis and turbulance and decrease of rate of blood flow-
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1.
- permits erythrocytes and platelets to come to contact with endothelial cells
2.
- permits a formation aggregates of platelets and fibrin, often in pockets of stasis
3.
- prevents dilution of clooting factors in plasma
4.
- decreases inflow of clotting factor inhibitors
5.
- promotes endothelial cell hypoxia and injury
Stasis play dominant role in thrombosis in veins because of low speed of blood flow in veins - origin of venous thrombi in sinuses behind venous valves in deep vein in low extremities similar phenomen- in auricular appendices of heart chambers - in atrial fibrillation
- stasis and turbulence contribute to thrombosis in arterial aneurysmal dilatations
-3- hypercoaguability of the blood -is defined as alteration of the blood and the clotting mechanism that predispose to thrombosis rare- good example is inherited lack of natural anticoagulant antithrombin
III- patients suffer of recurrent thromboembolic attacks
thrombotic diathesis in several chronic diseases - such as
- nephrotic syndrome
- late pregnancy
- disseminated cancer
-use of oral contraceptives- increase in plasma level of prothrombin, fibrinogen and other coagulative factors can be demonstrated
-trauma, surgery, burns
-cardiac failure
-advanced age, immobilization and reduced physical activiy increase the risk of venous thrombosis
MORHOLOGY OF THROMBI
-thrombi may develop in any part of cardiovascular system (heart, veins, arteries, capillaries)
 -arterial and cardiac thrombi: arise at sites of endothelial injury, atherosclerosis- often at the site of branching of the artery- white or mixed
thrombi- composed of fibrin white blood cells and erythrocytes
-mural thrombus- thrombus attached to one wall of the artery- mural thrombi also develop in abnormally dilated arteries-aneurysms
- occlusive thrombi - thrombus completely obstructs the lumen- in smaller arteries most commonly affected arteries: coronary, cerebral, femoral, iliac, mesenteric, popliteal
-venous thrombi: also known as „phlebothrombosis„- mural or occlusive
 -in slower-moving blood in veins- red coagulative or stasis thrombi composed mostly of fibrin and erythrocytes most commonly affected veins: veins of lower extremity (deep calf, femoral, popliteal, iliac), periprostatic plexus, portal vein etc venous thrombi can be confused with postmortem clots at autopsy
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 postmortem clots- are not attached to the endothelial surface, are rubbery and gelatinous, have smooth surface, do not contain platelets in contrast, thrombi are more firm, almost always have point of attachment, on the section show barely visible strands of fibrin
 -heart valvular thrombi : blood-borne infections may attack heart valves- endocardial damage- associated with development of thrombus - in bacterial or infective endocariditis less commonly- verrucous endocarditis-appear in patients with systemic lupus erytemathodes- autoimmune complex disease affecting skin, kidney and other organs nonbacterial or thrombotic endocarditis - in older patients with terminal cancers or severe malnutrition-marasmus
= marantic endocarditis- hypercoagulative state + minor endocaridial injury are leading pathogenetic aspects
DEVELOPMENT OF THROMBUS:
1. thrombus may continue to grow into adjacent vessels
2. thrombus may embolize
3. thrombus may be removed by fibrinolytic activities
4. it may undergo organization- when thrombus persists in situ for several days- it may be organized= ingrowth of granulation tissue and mesenchymal cells into the fibrinous thrombus
-thrombus is populated with spindle mesenchymal cells and capillary channels are formed within thrombus
-the surface of thrombus becomes to be covered by endothelial cells capillary channels anastomose- recanalization = reestablishing the continuity of original vessel
CLINICAL SIGNIFICANCE OF THROMBOSIS:
1. they cause obstruction, lead to infarction
2. they may provide the source of embolism
-superficial veins- varicosities, such thrombi may cause local edema and congestion and pain, rarely give rise to emboli, local edema predispose to infection-varicous ulcers difficult to heal
-deep veins of the leg (popliteal, femoral, iliac)- the most important source of emboli, they also may cause edema, pain, tenderness but approximately half of the patients with deep vein thrombosis are asymptomatic
EMBOLISM
Embolism refers to occlusion of a part of a cardiovascular system by impaction of embolus transported to the site of occlusion by blood stream
- most emboli represent parts of thrombi, thus the term thromboembolism,
-less commonly- other material such as fat droplets, gas bubbles, atherosclerotic debris, tumor fragments…
TYPES OF EMBOLISM:
1. pulmonary embolism
2. systemic embolism
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3. paradoxical embolism
 PULMONARY EMBOLISM: most common example of embolism- thrombus originates in venous system of legs, especially of deep leg veins, occasionally from right side of heart and embolus or emboli are transported into right heart ventricle and to pulmonary arteries pulmonary emboli may have various forms, morphologic and functional consequences of pulmonary embolism depend on the state of pulmonary circulation and the size of affected artery :
 -multiple small emboli in peripheric branches of pulmonary artery
-smaller emboli impact in medium-sized arteries- if cardiovascular circulation is normal, the vitality of lung tissue is maintained, but alveolar spaces are usually filled with erythrocytes= pulmonary hemorrhage
-with compromised cardiovascular status (in congestive heart failure)- hemorrhagic infarction
-Pulmonary infarction is sharply circumscribed necrosis of triangular shape with apex pointing towards the hilus of the lung
-pleural surface is covered with fibrinous exudate
 -large snake-like emboli--large emboli impact in main pulmonary arteriesdeath usually follows
 -saddle embolus-massive embolism in main pulmonary artery, death suddenly from hypoxia or right ventricle heart failure (acute cor pulmonale) - no time to develop morphologic changes in lung tissue
CLINICAL SIGNIFICANCE OF PULMONARY THROMBOEMBOLISM:
-many pulmonary emboli are clinically silent- small embolic mass is rapidly removed by fibrinolysis, or larger one may be subject of healing = organization of emboli - result in postembolic recanalization - healing
-recurrent multiple emboli= successive thromboembolism- may cause chronic hypertrophy of right ventricule and right-sided heart failure- chronic cor pulmonale (pulmonary hypertension and chronic right ventricle failure)
-embolic obstruction of middle-sized arteries- not infarction, but foci of hemorrhages- hemoptysis and dyspnoe
-obstruction of small peripheral arteries- usually cause infarctions
-massive pulmonary embolism-acute heart failure-sudden death
 SYSTEMIC EMBOLISM - is a embolism to systemic arteries, most commonly affected are - brain, kidney, spleen
Sources of the emboli for the systemic arteries:
- intracardiac mural thrombi (in myocardial infarction)
- atherothrombotic fragments from the aorta and the large arteries
-fragments of thrombi from the heart valves
-from the left heart atrium - in atrial fibrillation
-thrombi filling the left ventricle aneurysm
 PARADOXICAL EMBOLISM - most common source- clots in deep leg veins, and most common target organs- arteries of the brain, kidney, spleen abnormal opening between right and left atrium (foramen ovale), higher blood pressure on right side than on left allows embolization from systemic veins to systemic arteries
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 FAT EMBOLISM = is defined as lodgment of fatty droplets and minute globules of fat in blood capillaries fat embolism appears as a complication of bone fractures -fragments of fatty bone marrow, soft tissue traumas and burns
-about 90% patients with severe skeletal injuries have fat embolism, but very few have clinical course known as fat embolism syndrom - acute respiratory insufficiency, neurological symptoms, anemia and thrombocytopenia - typically syndrom appears about 2 - 3 days after injury the fat embolism syndrome has mortality of about 10% pathogenesis of fat embolism syndrom- not absolutely clear, both mechanical obstruction and chemical injury are involved microaggregates of fat cause occlusions in microcirculation of lungs and brain and free fatty acids cause endotheial cell damage - microglobules of fat are found in capillaries in many organs- most important- brain
 AIR EMBOLISM ( including CAISSON DISEASE )
= is defined as entry of air into venous or arterial blood vessels
-in venous air embolism- small quantities are innoculous, but 100 ml and more may be fatal
-in arterial air embolism- even small quantity may be fatal, most commonly - complication of abortion, chest surgery
 caisson disease is a particular form of gas embolism =decompression
sickness may appear in deep-sea divers who ascend rapidly to high altitudes, the gases within pressurized air are dissolved in the blood, tissues and fat if the diver then ascends up rapidly to the surface- the dissolved oxygen, nitrogen and carbon dioxide come out of solution in the form of small bubbles
-most dangerous in this respect seems to be nitrogen, because of its low solubility- nitrogen persists as gas bubbles
- mainly in the brain - brain necroses
-the same process may affect other highly vascularized tissues and organs, such as heart and kidney, skeletal muscles, etc.
-in the lungs- sudden respiratory distress syndrom
TREATMENT: rapid placing of the affected person into the compression chamber- and slow decompression
 AMNIOTIC FLUID EMBOLISM -is characterized by sudden onset, rapid dyspnea, cyanosis, collapse and coma with convulsions occurs rarely, is totally unpredictable, may be fatal - is one of major causes of maternal death after delivery typical findings: in pulmonary arteries and capillaries- epithelial squames from fetal skin, lanugo hairs, fibrin thrombi indicative of DIC - in small vessels of uterus, lungs, kidney, thyroid, myocardium pathogenesis of amniotic fluid embolism is unclear the main cause of syndrom is infusion of amniotic fluid into the blood, such entry may occur through cervical uterine veins, from the uteroplacental site , etc
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it is suspected that vasoactive substances from the amniotic fluid are responsible for pulmonary vasocontriction
-thrombogenic substances from amniotic fliud- may cause intravascular coagulation leading to DIC hemorrhages and acute renal failure
 DISSEMINATED INTRAVASCULAR COAGULATION ( DIC)
= is characterized by activation of coagulation sequence that leads to formation of multiple minute fibrin thrombi in capillaries and small venules
-the thrombi are mostly composed of fibrin and aggregations of platelets this leads to widespread thromboses with consumption of platelets and of coagulation factors and with subsequent fibrinolysis (secodary effect)- DIC is also called microvasculary thrombosis thromboses cause focal ischemia - multiple foci of necrosis mostly in the lungs, kidneys, brain, heart
-increased bleeding tendency causes multiple hemorrhages
 main clinical disorders associated with DIC:
DIC is not primary disease, it is a complication of some underlying diseases , such as
-amniotic fluid embolism
- EPH gestosis
- septic abortion
-retained dead fetus or abruption placentae
-severe infections ( gram-negative sepsis for example )
-neoplasms, such as carcinoma of pancreas, prostate, lungs
-massive tissue injury, burns
-extensive surgery, etc
 morphology of DIC: widespread occurrence of fibrin thrombi in capillaries of kidney, adrenal glands, brain, and other organs
-ischemia and multiple microinfarcts
-necrosis in adrenals may cause Waterhouse-Fridrichsen syndrom
-necrosis in brain- severe neurologic complications
-DIC leads to hemorrhagic diathesis, because of consumption of clotting factors in multiple microthrombi increased bleeding tendency causes multiple hemorrhages
INFARCTION. SHOCK
 INFARCTION
-infarct is a localized ischemic necrosis in an organ or tissue resulting from sudden occlusion of arterial supply
CAUSES OF INFARCTIONS:
-thrombotic or embolic occlusions-
1. thrombosis = in situ formation of blood clot that occludes lumen of blood vessel
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2. embolism = a portion of the thrombus in one area breaks off and lodges into the blood vessel of the other area usually of narrower lumen less common causes of infarcts include:
3. atherosclerosis = narrowing of lumen or the total obstruction of the lumen by atherosclerotic plaque alone- due to ulceration, hemorrhage, or edema of the plaque
4. spasm of artery = due to active pathologic vasocontriction
5. hypotension - causes severe temporary impairments of blood supply in an area of compromised circulation
6. twisting of the blood vessel with occlusion of both arteries and veins
-in a hernial sac or under peritoneal adhesion
-in cases of torsion of organs or tissues that have the blood supply through a pedicle, such as ovaries, testes
7. pressure of blood vessel - caused by expanding tumor or due to mechanical pressure in decubital ulcer
 MORPHOLOGY OF INFARCTS:
Infarcts can be divided into two types:
-white (anemic)
-red (hemorrhagic) the distinction is given only by amount of hemorrhage that occurs in necrotic area, the difference is not principal
1. WHITE, PALE INFARCTS
- in solid organs (heart, spleen, kidney)- firm consistency of the organ does not permit blood inflow into the necrotic area
2. RED, HEMORRHAGIC INFARCTS
- in loose, spongy tissues (lungs, intestine) permits blood to collect in necrosis from the anastomosing capillary circulation -
-hemorrhagic infarcts are also encountered if the venous outflow from the necrotic area is limited -for example hemorrhagic venous infarction of intestine
-in some intstances, spasm of vessels about clot subsequently relaxes causing partial hemorhagic infarction
all infarcts ( white and red )- tend to be wedge shaped, occluded vessel is at the apex of necrosis and the periphery of the organ forming the base of infarct
-the adjacent serosal surface is covered with fibrinous exudate
 MORPHOLOGY OF DEVELOPING INFARCT:
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1- at the onset- all infarcts tend to be poorly defined and slightly hemorrhagic due to anoxic leakage of residual blood from capillaries in affected area - early infarcts are grossly red
2- at later stage- white infarcts in solid organs- (spleen, kidney) become well circumscribed, progressively pale, sharply delimited with hyperemic border -
-hemorrhagic infarcts in spongy organs - (lung, intestine), first the infarct is cyanotic, later is firmer and brown (hemosiderin deposits), the delimitation of infarcts- inflammatory reaction and hyperemia at the margins of necrosis
-in organs with excellent collaterals- the infarction remains red because blood continues to be poured to the affected area
-in venous occlusion- infarction is usually hemorrhagic
-in heart- appearance may be mixed red and white, yellow color is due to accumulation of leukocytes
-in brain- cerebral infarction usually undergoes liquefaction
3- at last stage -in most organs, the infarcted area is replaced by granulation tissue which is finally replaced by a scar with deposits of hemosiderin scars
-in lungs- infarcts dry out, become paler eventually are replaced by
-in heart - a similar phenomen occurs, but solid consistency of heart muscle does not permit great shrinkage and even prominent scar is of normal size (myofibrosis)
-in brain- scars do not from in the brain, and the necrotic area liquefies. As a result, a speudocyst may be formed- smooth-walled, glia-lined cavity (postmalatic pseudocyst)
-in intestine- infarction causes death if not removed surgically- no
development
FACTORS THAT INFLUENCE THE DEVELOPMENT OF INFARCT
 1- nature of vascular supply
-the most important is an availability of alternative way of blood supply in the affected area - role of collateral circulation
-in organs with abundant collateral circulation (notably the lungs)- arterial occlusion leads to development of infarct only if preexisting vascular disorders (usually congestive heart failure) is present
the lungs have dual arterial supply (pulmonary system and bronchial arterial supply)
-occlusion of small branch of pulmonary artery in young person with normal bronchial circulation does not produce infarct
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-embolism in older person with pulmonary hypertension and pulmonary congestion, emboli often result in hemorrhagic infarcts
in liver- similar situation with dual circulation- hepatic and portal arterial system
upper extremity-double arterial supply through radial and ulnar arteries- of the hand and forearm- prevents development of infarction or gangrene of this extremity, this is not true for legs
heart- collateral circulation- may operate even in coronary circulation- important in preventing myocardial infarction
-three major coronary arteries (left anterior descending, left circumflex and right coronary artery)- effective small anastomoses between these three trunks
 2- rapidity of occlusion
-slowly developing occlusions-usually cause vascular atrophy, very seldom cause infarct - since they provide opportunity to improve or develop the alternative blood supply,
-rapidly developing occusions-more likely to cause infarct
 3- vulnerability of tissue to hypoxia the susceptibility of a given tissue to hypoxia influence the likelihood of infarction neurons and nervous tissue- irreversible damage even after 4-5 min of anoxia muscle myocardial cell also very sensitive to hypoxia in contrast, less sensitive are fibroblasts, lipocytes, skeletal many epithelial cells- resistent to hypoxia
 4-oxygen-carrying capacity of blood patients with normal levels of oxygen transport tolerate better disorders of vascular supply, than those with anemia or cyanosis
-thus, cardiac failure can contribute to development of infarct through reduced level of oxygen transport capacity
 SHOCK
= acute circulatory deficiency caused by inadequacy or maldistribution of blood supply resulting in circulatory hypovolemia
-may develop following any massive insult to the body, constitutes a widespread hypoperfusion of cells and tissues due to reduction of blood volume or due to redistribution of blood resulting in a considerable decrease of effectiveness of circulation.
-leads to serious tissue ischemia, irreversible injuries and may eventually cause the death of patient
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TYPES OF SHOCK:
1. CARDIOGENIC = shock related to cardiac pump failure
-caused by heart muscle damage (myocardial infarction, rupture of heart), or rhythmic disorders, (arrhytmias), and pulmonary embolism, cardiac tamponade, etc.
2. HYPOVOLEMIC- results from either internal or external fluid loss
-both hypovolemic and cardiogenic shock cause a drop in cardiac output and a decrease in tissue perfusion
3. HEMORRHAGIC SHOCK
-blood loss may be - external or internal
-may be initiated by trauma or endogenous (spontaneous) resulting from ulcerating or necrotizing lesions, such as- disruption of artery wall in peptic ulcer
-bleeding from arteries due to tumor invasion
-bleeding from varices- esophageal in liver cirrhosis
-from dissecting or saccular arterial aneurysm
-fluid loss (excessive vomiting, diarrhea, burns)
4. BURN SHOCK= massive loss of fluid and blood cell into injured tissue and from denuded surface
-Mechanisms underlying cardiogenic and hypovolemic shock-low cardiac output, hypotension, decreased tissue perfusion, tissue hypoxia
5. SEPTIC = shock related to severe bacterial infections, (particularly gramnegative bacilli, such as Escherichia coli, Klebsialla pneumoniae)- gram-positive bacteria, such as streptococci, pneumococci
-endotoxemia secondary to sepsis causes increased vascular permeability and internal loss of fluids from the circulation
Mechanisms underlying septic shock less obvious - in majority of cases -
endotoxins and DIC are most important in pathogenesis.
6. ENDOTOXIC SHOCK
-cardiac output is not lower, but the capacity of arterial system is abnormally incresed due to arterial dilatation
-septic shock is associated with defects of distribution of blood- so called peripheral pooling, with endotoxin-mediated activation of inflammatory responce and direct toxic damage to the tissues
7. NEUROGENIC - after anesthesia, and in spinal cord injury major mechanism is peripheral vasodilatation with pooling of blood
PATHOLOGY AND PATHOGENESIS OF SHOCK :
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-whatever the main cause leading to shock is, major pathogenetic
aspect is diminished volume of circulating blood
-due to loss of extracellular fluid or due to blood loss
- due to pooling of blood in certain areas, such as in the abdominal viscera in abdominal trauma
STAGES OF SHOCK:
1- nonprogressive stage-reflex compensatory mechanisms are activated and perfusion and blood supply to vital organs is preserved
2- progressive stage -is characterized by tissue hypoperfusion, progressive tissue hypoxia due to arterial dilatation and stasis, function of vital organs begin to deteriorate- the patient is confused
3- irreversible stage - is characterized by irreversible tissue injury of hypoxia, condition no longer responsive to therapy
-the flow through the renal cortex is markedly reduced - renal tubular necrosis develops, with consequent decrease in the urinary output- resulting in metabolic acidosis
 MORPHOLOGIC CHANGES DUE TO SHOCK:
-tissue changes are essentially the same as those of hypoxic injury,
-late stages of shock are characterized by failure of multiple organs
brain-ischemic encephalopathy- changes due to ischemia and hypoxia changes depend on the duration of hypoxia
-in mild cases- transient confusional state, more severely affected patients will be comatose with subsequent loss of part of cortical function
heart -variety of changes- myocardial infarction, subendocardial hemorrhage,
lungs- so called shock lung - Adult respiratory distress syndrome ARDS,
-ARDS is a clinical syndrome not always but often associated with shock,
-grossly. the lungs are firm, dark red, airless, heavy
-microscopically: capillary congestion, intraalveolar edema and hemorrhage, fibrin thrombi may be presentin capillaries, diffuse alveolar damage, hyaline membranes lining the alveolar surfaces,
kidneys-acute tubular necrosis
adrenal glands- focal depletion of lipids in the cortical cells-this loss of corticolipids does not imply adrenal exhaustion, but more likely activated state and increased production of corticoids
gastrointestinal tract -focal mucosal hemorrhages
liver-fatty change or centroacinar necroses
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