Typical disorders of peripheral blood flow

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prepared by MD, PhD Marta R. Gerasymchuk, pathophysiology department of Ivano-Frankivsk National Medical University

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  • There are two groups of disorders of peripheral blood flow.
  • In this lecture we review the disorders of local peripheral flow.
  • Blood flow disturbances in the vessels of medium diameter can be classified as pathological, arterial hyperemia, venous hyperemia, ischemia and stasis.
  • Microcirculation is a regular flow of blood and lymph through microvessels, transport of transcappilary plasma and blood corpuscles, fluid transfer outward vessels.
    Microcirculatory bed. A number of arterioles, capillaries and venules form a structural and functional unit of the cardiovascular system, namely, a microcirculatory(terminal) bed. A terminal bed is structured as follows. A metarteriole branching into anastomizing actual capillaries forming a network branches from the terminal arteriole. The venous part of capillaries continues to precapillary venules.
    At the site where a capillary branches from an arteriole there is a precapillary sphincter – accumulation of circularly oriented smooth muscle cells. Sphincters control local blood volume passing through actual capillaries. Blood volume passing through the terminal vascular bed is determined by arteriole tone of smooth muscle cells. Arteriolovenular anastomoses, connecting arterioles directly to small veins (juxtacapillary blood flow) are also in themicrocirculatory bed.
    Walls of anastomosis vessels contain many smooth muscle cells. Arteriovenous anastomoses are present in large quantities in some areas of the skin where they play an important role in temperature regulation(lobule of the ear, fingers). Small lymph vessels and intercellular spaces are also part of the microcirculatory bed.
  • Distinguish three groups of reasons of disorders of hemomicrocirculation
    Three groups of typical forms of microcirculation disturbances are classified as follows: intravascular, transmural and extravascular. Microcirculation disturbances cause capillary trophic insufficiency,
    Causes of microcirculation disturbances
    Numerous causes including various microcirculation disturbances are classified into three groups.
    Central and regional circulatory disturbances. The major ones are cardiac insufficiency, pathological forms of arterial hyperemia, venous hyperemia, ischemia.
    Changes of viscosity and blood and lymph volume develop as a result of hemoconcentration and hemodilution.
    Hemo (lympho) concentration. Causes: hypohydration of the body associated with developing polycythemic hypovolemia, polycythemia, hyperproteinemia (mainly hyperfibrinogenemia).
    Hemo (lympho) dilution. Causes: hyperhydration of the organisms associated with developing oligothemic hypervolemia, pancytopenia (decreased quantity of all blood corpuscles), increased aggregation and agglutination of blood corpuscles ( resulting in a significant increase of blood viscosity), DIC - syndrome (disseminated intravascular coagulation).
    Damage of vascular walls in the microcirculatory bed.
    It is usually observed in atherosclerosis, inflammation, cirrhosis, tumours, etc.
  • Intravascular disturbances of microcirculation
    Typical forms of intravascular disturbances of microcirculation
    Slow rate (up to stasis) of blood and lymphatic flow is the major cause. This may be causes by hemo- and lymphodynamics disturbances (e.g. in cardiac insufficiency, venous hyperemia ischemia).
    Increased blood and lymph viscosity as a result of hemo- (lympho-) concentration due to prolonged vomiting, diarrhea; plasmorrhagia due to burns, polycytemia, hyperprotenemia, blood cell aggregation, intravascular coagulation, microthrombosis. Significant narrowing of a microvascular lumen (squeezed by a tumour, edematic tissue, caused by formation of thrombi or potentiation of an embolus, swelling or hyperplasia of endothelial cells, atherosclerotic plaque formation, etc).
    Manifestations are similar to those which are observed in the vessels of microcirculation in venous hyperemia, ischemia and stasis.
    Blood flow acceleration.
    The major causes.
    Hemodynamic disorders (e.g. in arterial hypertension, pathological arterial hyperemia or discharge of arterial blood into the venous stream through arteriovenular shunts.
    Blood viscosity reduction due to hemodilution (in water intoxication); hypoproteinemia, renal insufficiency (at an oliguric or anuric stage); pancytopenia.
    Disturbed blood and/or lymph flow turbulence.
    The most common causes.
    Changes of blood viscosity and state of aggregation (as a result of formation of blood cell aggregates when the increased number of blood corpuscles exceeds the norm or in hyperfibrinogenemia or in case of microthrombus formation).
    The damage of the walls of microvessels affecting their smoothness in vasculitis, hyperplasia of endothelial cells, atheriosclerosis, fibrous changes in different layers of vascular walls, tumour development in them, etc.)
    Increased juxtacapillary blood flow. It occurs when arteriolovenular shunts are opened and blood is discharged from arterioles into venules avoiding capillary network of the microcirculatory bed.
    The cause: spasm of smooth muscle arterioles and closure of precapillary sphincters as in case of an increase in catecholamine content in blood (e.g. in hypercatecholamine crisis in patients with pheochromocytoma), or in case of a significant increase of the sympathetic nervous system tone (e.g. in stress situations), or in case of hypertensive crisis (e.g. patients with hypertension).
    Manifestations: ischemia in the area where blood is discharged from arterioles into venules, opening and/or increase of the diameter of arteriovenular shunts. Turbulent character of blood flow at the sites where the shunting vessels branch from or enter venules which is conditioned by the fact that arteriovenular shunts branch from arterioles and enter venules, as a rule, at a considerable angle; it is accompained by the process in the course of which blood corpuscles strike one another and vascular walls, which results in proaggregate and procoagulant release and aggregate and thrombus formation).
  • Emigration disturbances. In different pathological conditions the number of blood corpuscles passing through vascular walls may increase or decrease.
    Leucocyte emigration through microvascular walls also occurs in the normal state. Excessive leucocyte emigration, thrombocyte and erythrocyte release from blood followed by microhemorrhages are considered pathological.
  • Transmural disturbances of microcirculation
    Either a fluid part of blood (in this case we deal with permeability) or cell elements (in this case we deal with emigration) may pass through walls of microvessels. According to the prevalence either of permeability or of emigration transmural disturbances are subdivided into two categories: permeability disturbances and emigration disturbances.
    Permeability disturbances. In different pathological conditions volume of blood plasma and/or lymph passing through a vascular wall can increase or decrease.
    Increased permeability.
    The major cause of increased permeability of the walls of microvessels
    Consequences. Increased permeability of microvascular walls activates the mechanisms of fluid transfer: filtration (fluid transport according to hydrostatic pressure gradient); diffusion (fluid transport which does not involve any energy losses); osmosis directed fluid diffusion according to osmotic pressure gradient).
    Decreased permeability
    Causes: thickening and/or induration of the vascular walls, or disturbances of energy supply of intracellular processes.
    Consequences. Decreased efficiency of fluid transfer mechanisms: filtration, diffusion, transcytosis, osmosis.
  • Transmural disturbances of microcirculation
    Either a fluid part of blood (in this case we deal with permeability) or cell elements (in this case we deal with emigration) may pass through walls of microvessels. According to the prevalence either of permeability or of emigration transmural disturbances are subdivided into two categories: permeability disturbances and emigration disturbances.
    Permeability disturbances. In different pathological conditions volume of blood plasma and/or lymph passing through a vascular wall can increase or decrease.
    Increased permeability.
    The major cause of increased permeability of the walls of microvessels
    Consequences. Increased permeability of microvascular walls activates the mechanisms of fluid transfer: filtration (fluid transport according to hydrostatic pressure gradient); diffusion (fluid transport which does not involve any energy losses); osmosis directed fluid diffusion according to osmotic pressure gradient).
    Decreased permeability
    Causes: thickening and/or induration of the vascular walls, or disturbances of energy supply of intracellular processes.
    Consequences. Decreased efficiency of fluid transfer mechanisms: filtration, diffusion, transcytosis, osmosis.
  • Extravascular disturbances of microcirculation
    Extravascular disturbances of microcirculation are accompanied by increased or decreased volume of intracellular fluid which results in its slower flow into microcirculatory vessels.
    Increased volume of intracellular fluid coupled with its slower flow from the interstitial space.
    The cause: local pathological processes (inflammation, allergic reactions, newgrowth, sclerotic processes, venous hyperemia and/or stasis).
    Consequences.
    Increased content of the products of normal and disturbed metabolism in the interstitial fluid. They can have a cytotoxic and cytolytic effect.
    Ion imbalance (causing tissue edema, disturbing membrane rest potential and action potential formation).
    The formation of excessive biologically active substances or their activation (e.g. tumor necrosis factor, procoagualants) which can cause a more severe damage of cells, initiate blood and lymph circulation disturbances, plastic process.
    Disorders of O2, CO2 metabolism, metabolism of substrates and metabolites.Cell compression by excessive interstitial fluid.
    Increased volume of intracellular fluid followed by disturbances of its outflow from interstitial space.
    Causes:
    Hypohydration of the organism, tissues and organs (e.g. as a result of prolonoged diarrhea, plasmorrhagia, profuse sweating).
    Reduced lymph formation (e.g. in tissue ischemia or hypovolemia).
    Decreased efficiency of fluid filtration in arterioles and precapillaries and/or its increased reabsorbtion in postcapillaries and venules (e.g. in dystrophic and sclerotic processes in tissues).
    Consequences are similar to those which are observed when the volume of the intestinal fluid increases and its outflow becomes slower (see the above-stated information).
    Capillarotrophic insufficiency.
    Capillarotrophic insufficiency is a state characterized by blood and lymph circulation disturbances in the vessels of microcirculation, disorders of fluid and blood corpuscles transport through the microcircular walls, slower outflow of the intracellular fluid and metabolic disorders in tissues and organs
    As a result of the above-stated changes different types of dystrophy develop, plastic (flexible) processes in tissues are impaired, vitality of organs and the body in general decreases.
  • Pathophysiology of edema
    1. Alteration in Starling pressure
    a. Produces a transudate
    b. Clinical examples of increased vascular hydrostatic pressure
    1) Pulmonary edema in left-sided heart failure
    2) Peripheral pitting edema in right-sided heart failure
    3) Portal hypertension in cirrhosis producing ascites
    c. Clinical examples of decreased vascular plasma oncotic pressure (hypoalbuminemia)
    (1) Malnutrition with decreased protein intake
    (2) Cirrhosis with decreased synthesis of albumin
    (3) Nephrotic syndrome with increa.sed loss of protein in urine (>3.;ig/24 hours)
    (4) Malabsorption with decreased reabsorption of protein
    d. Renal retention of sodium and water
    (1) Increases hydrostatic pressure (increased plasma volume)
    (2) Decreases oncotic pressure (dilutional effect on albumin)
    (3) Examples—acute renal failure, glomerulonephritis
    2. Increased vascular permeability
    a. Produces an exudate
    b. Fxample—acute inflammation (e.g.. tissue swelling following a bee sting)
    3. Lymphatic obstruction
    a. Produces lymphedema
    b. Examples
    (1) Lymphedema following modified radical mastectomy and radiation (see l-'ig. 'KS)
    (2) Filariasis due to Wucherreria bancrofti
    (3) Scrotal and vulvar lymphedema due to lymphogranuloma venereum
    (4) Breast lymphedema (inflammatory carcinoma) due to blockage of subcutaneous lymphatics by malignant cells
    4. Increased synthesis of extracellular matrix components (e.g., glycosaminoglycans)
    a. T-cell cytokines stimulate fibroblasts to synthesize glycosaminoglycans,
    b. Example—pretibial myxedema and exophthalmos in Graves' disease
  • The movement of fluid between vascular and interstitial spaces is controlled mainly by the opposing effects of vascular hydrostatic pressure and plasma colloid osmotic pressure.
    Normally, the exit of fluid into the interstitium from the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end;
    the lymphatics drain a small residual amount of excess interstitial fluid.
    Either increased capillary pressure or diminished colloid osmotic pressure can result in increased interstitial fluid.
    As extravascular fluid accumulates in either case, the increased tissue hydrostatic and plasma osmotic pressures eventually achieve a new equilibrium, and water re-enters the venules.
    Excess interstitial edema fluid is removed by lymphatic drainage, ultimately returning to the bloodstream via the thoracic duct ; clearly, lymphatic obstruction (e.g., due to scarring or tumor) can also impair fluid drainage and cause edema.
    Finally, sodium retention (with its obligatory associated water) due to renal disease can also cause edema.
  • Tissue hematomas and hemorrhages (internal and external) resulting from overdistention and microruptures of venous vessel walls (postcapillaries and venules).
    Changes in the vessels of microcirculatory bloodstream.
    Increased diameter of capillaries, postcapillaries and venules resulting from the distension of microvessel walls due to venous blood excess.
    Increased number of functioning capillaries at the initial stage of venous hyperemia (resulting from venous blood outflow through earlier non-functioning capillary network) and their reduced number at further stages (due to blood flow arrest as a result of formation of microthrombus and blood cell aggregates in postcapillaries and venules).
    Slow rate or even arrest of venous blood outflow.
    Significant dilation of the axon diameter and disappearance of plasma flow in venules and veins.
    Pendular movement of blood in venules and veins.
    “Forward” - from capillaries to venules and veins. Caused by propagation of a systolic wave of cardiac output.
    “Backward” - from veins to venules and capillaries. Caused by the fact that venous blood flow rebounds from the mechanical barrier (thrombus, embolus, constricted (narrowed) site of the venule).
  • Its typical pathological process, what characterized by disorders of blood flow in vessels, diameter of them is more 100 micrometers.
  • Physiological arterial hyperemia
    Physiological arterial hyperemia has an adaptive meaning. It can be functional and protective.
    Functional hyperemia develops in organs and tissues due to their increased activity (e.g. hyperemia in a contracting muscle or in a highly active organ).
    Protective hyperemia develops when protective reactions and processes are in progress (e.g. in the inflammation focus, or around a foreign graft (transplantant), necrotic zone, or bleeding zone). In this case arterial hyperemia induces the transport of oxygen, metabolic substrates, Igs, phagocytes, lymphocytes to tissues and other cells and agents essential for local protective and restorative reactions.
    Pathological arterial hyperemia
    Pathological arterial hyperemia doesn’t involve any changes of organ and tissue functions but impairs adaptability and causes damage.
    Pathological arterial hyperemia is associated with impaired blood supply, microhemocirculation, transcapillary metabolism, sometimes by hemorrhages.
  • Neuroparalytic mechanism.
    the depletion of catecholamine deposits in synoptic vesicles of varicose terminal sympathetic nervous fibers in the wall of arterioles;
    the reduction of the smooth muscle tonus of arterial vessels
  • Metabolic and oxygen supply disorders may cause hypertrophy and hyperplasia.
    It is the effects of arterial hypertensions which a number of treatments are targeted at (e.g. the administration of compresses, mustard plasters, physiotherapeutic treatments; injections of vasodilators; in surgeries for transecting sympathetic nerve trunks and excising sympathetic ganglia in certain types of angina pectoris, etc.) All these treatments are aimed at inducing hyperemia.
    These treatments are administered in case of organ and tissue damage, their ischemia, impaired trophism and plastic processes in them, decreased local immunity.
    Overextension and microrupture of vascular walls of microcirculatory bloodstream, micro- and macro- hematomas, internal and external hemorrhages in tissues are observed in pathological types of arterial hyperemia. The aim of arterial hyperemia therapy is to eliminate and prevent these negative effects.
  • Increased number and diameter of arterial vessels at the site of arterial hyperemia.
    Reddening of an organ, tissue or their site due to increased flow of arterial blood, dilatation of the lumen of arterioles and precapillaries, increased number of functioning capillaries, arterialization[vascularization] of venous blood (i.e. increase of HbO2 level in venous blood).
    The temperature
    The t0 increase of tissues and organs at the site of hyperemia results from warmer arterial blood flow and higher metabolic intensity.
    Increased lymphopoiesis and lymph outflow due to increased perfusion pressure in the vessels of the microcirculatory bloodstream.
    Increased volume and turgor of an organ or tissue as a result of their higher blood and lymph volume.
    Changes in the vessels of microcirculatory bloodstream.
    An increase of the diameter of arterioles and precapillaries
    Increased number of functioning capillaries (i.e. capillaries through which plasma and blood corpuscles flow).
    Accelerated blood flow through microvessels.
    Reduced diameter of the axon (blood cell flow along the central axis of an arteriole) and increased width of plasma flow containing small amounts of blood corpuscles around this axon. It is caused by increased centripetal forces bouncing blood cells to the center of the lumen of vessels as blood flows faster as in case of arterial hypertension.
    The effects of arterial hyperemia
    Activation of the specific function (functions) of an organ or tissue and potentiation of their non-specific functions and processes are observed in various physiological types of arterial hyperemia.
    Example: activation of local immunity (due to increased flow of Ig, lymphocytes, phagocytizing cells and other agents with arterial blood), acceleration of plastic processes, increase of lymphopoiesis and lymph outflow from tissues.
  • The major cause of venous hyperemia is a mechanical obstruction hindering venous blood outflow from tissues or organs. It may be caused by a narrowed lumen of a venule or a vein when it is compressed (by a tumor, edematic tissue, a scar, a tourniquet, a tight bandage) and obturation (by a thrombus, embolus or tumor); cardiac insufficiency, low elasticity of venous walls associated with the formation of dilatated or constricted sites in them.
  • Increased diameter of the lumen of venous vessels and their number at the site of hyperemia.
    Tissue and organ cyanosis due to increased venous blood volume in them and reduced HbO2 level in the venous blood. The latter is the result of the utilization of oxygen taken by tissues from the blood due to its slow flow through capillaries.
    Reduced temperature of tissues and organs at the site of venous (passive) congestion resulting from increased volume of colder (in comparison with arterial blood) venous blood and lower intensity of tissular metabolism (resulting from reduced arterial flow to tissues at the site of venous hyperemia).
    Tissue and organ edema occurs due to increased intravascular pressure in capillaries and venules. In case of prolonged venous hyperemia edema is potentiated by its osmotic, oncotic and membranogenic pathogenetic factors
  • Venous hyperemia damages tissues and organs which is caused by a number of pathogenic factors.
  • Mechanisms of ischemia development.
    Mechanisms causing a reduction of arterial blood flow to tissues and organs may be neurogenic, humoral and mechnical.
    Neurogenic mechanism (neurotonic and neuroparalytic).
    Neurotonic mechanism is characterized by the prevalence of the sympathetic nervous system effects on the walls of arterioles in comparison with those of the parasympathetic one. It also involves increased output of noradrenaline from adrenogenic terminals. Causes: activation of the sympathetic effects on tissues and organs (e.g. in various types of stress, exposure of tissues to low temperatures, mechanical trauma, chemical substances) and enhanced adenoreactive properties of arteriole walls (e.g. during their sensibilization to vasoconstrictive agents - in conditions of increased Ca2+ level or cyclic adenosine monophosphate in myocytes).
    Neuroparalytic mechanism is characterized by elimination or reduction (“paralysis”) of parasympathetic effects on the walls of arterioles. Cause: inhibition or blockade of nervous impulse propagation through parasympathetic fibers to arterioles (so that acetylcholine release from nerve fibers in the walls of the arteries, arterioles and precapillaries occurs). This can be observed in case of neuritis, mechanical traumas, tumor development, ganglionectomy or transection of parasympathetic nerves.
    Humoral mechanism is characterized by increased level of substances having a vasoconstrictive effect in tissues (e.g. angiotensin II, alcohol dehydrogenase, thromboxane A, adrenaline, prostaglandin) and sensitivity of receptors of arteriole walls to the agents having a vasoconstrictive effect (e.g. when [Ca2+] or [Na+] increases in tissues).
    Etiological factor of mechanical character. It is characterized by the presence of a mechanical obstruction to the blood flow through arterial vessels. Causes: compression of an arterial vessel by a tumor, a scar, edematic tissue, a tourniquet or narrowing (or even complete obturation) of an arteriole lumen (e.g. by a thrombus, aggregates of blood cells, an embolus).
  • Examples:
    Pathological arterial hyperemia of the brain in hypertensive crisis.
    Pathological arterial hyperemia of different organs and tissues developing according to the neuromyoparalytic mechanism (e.g. in the organs of the abdominal cavity after ascites, in the skin and muscles after a tight tourniquet is removed; at the site of chronic inflammation; at the site which was exposed to heat for some hours (sun heat, hot-water bottle; mustard plaster application) in the area of sympathetic denervation).
  • Types of stasis.
    All types of stasis are divided into primary and secondary ones.
    Primary actual stasis. Primary stasis formation starts from the activation of corpuscular blood elements releasing a large quantity of proaggregants and/or procoagulants. At the next stage the corpuscular elements of blood aggregate, agglutinate and attach to the walls of a microvessel. This causes inhibition or arrest of blood flow through vessels.
    Secondary stasis (ischemic and congestive)
    Ischemic stasis develops as an outcome of severe forms of ischemia due to decreased arterial blood flow reduction, slower rate of its flow, or its turbulent character. This leads to aggregation and adhesion of blood cells.
    Congestive (venous congestive) variant of stasis results from slower rate of venous blood outflow, pachyemia, changes of physical and chemical properties, damage of the blood corpuscles (particularly, due to hypoxia). Subsequently, blood cells adhere to one another and to the walls of microvessels.
  • Pathogenesis
    The final stage of stasis involves the process of aggregation and agglutination of the corpuscular elements of blood which results in blood thickening and its fluidity reduction. This process is activated by proaggregants, cations and high molecular weight proteins.
    Proaggregants (thromboxane A, adenosine phosphate, prostaglandin, prostaglandin E, catecholamines, AT to corpuscular elements of blood) cause adhesion, aggregation, agglutination of the corpuscular elements of blood followed by their lysis when biologically active substances are released from them (including proaggregants, stimulating aggregation and agglutination).
    Cations: K+, Ca2+, Na+, Mg2+ are released from blood cells, the affected walls of vessels and tissues. The excess of cations, absorbing on the cytolemma of the corpuscular elements of blood, neutralizes their negative superficial charge or even changes it for the opposite. While unaffected cells (due to the negative charge) rebound from one another, affected cells (“neutralized”) form aggregates. “Recharged” blood cells aggregate more actively. Having a positive superficial charge they approach neutralized cells, mainly, affected ones (with a negative charge), forming aggregates adhering to the intima of vessels (the inner coat of vessels).
    High molecular weight proteins (e.g. y-globulins, fibrogen) change the superficial charge of unaffected cells (getting into contact with the negatively charged cell surface with the help of positively charged amino group) and stimulate aggregation of formed blood elements and adhesion of their conglomerates to the vascular wall (this is achieved by fixation of a great number of protein mycells having adhesive properties on the surface of the formed blood elements).
  • Embolus and embolism.
    Embolus is a mass, circulating in cardiac cavities, in blood and lymph vessels, which doesn't occur in the normal state:
    Emboli may be endogenous and exogenous according to their origin, and arterial and venous according to their localization in vessels.
    Exogenous emboli: they are mostly air bubbles (getting into large veins when damaged/wounded) or foreign bodies (e.g. bullet splinters or oil-base drugs when they infused in a cold state).
    Endogenous emboli are as follows:
    fragments of thrombi (thromboemboli);
    portions of fatty tissue or bone forming during organ growth or tubular bone fractures;
    small fragments of disintegrating tumour tissue or destroyed normal tissue.
    Conglomerates of microbial cells, multicellular or unicellular (single-cell) parasites.
    Gas bubbles, normally soluble in the blood plasma, but forming as a result of a rapid drop of pressure - during plane or spaceship depressurization as well as when rising from a depth.
    Arterial emboli obstruct arterial vessels of the systemic circulation (penetrate from pulmonary veins or left heart chambers or veins of systemic circulation).
    Venous emboli are often found in small venous vessels of the portal vein.
    Embolism is circulation of a plug in the bloodslream and lymphatic flow, it doesn't occur in the normal state, and obstruction or constriction of a blood or lymph vessel by a plug.
  • 1 Causes of fat embolism
    a. Most often due to traumatic fracture of the long bones (e.g.. femur) or pelvis
    b. Other causes include trauma to fat-laden tissues (liposuction), fatty liver.
    2. Pathogenesis
    a. Microglobules of fat from the bone marrow gain access to the microvasculature.
    b. Microglobules eventually obstruct the microvasculature in the brain, lungs, kidneys, and other sites.
    • Produces ischemia and hemorrhage
    c. Fatty acids derived from breakdown of the microglobules damage vessel endothelium.
    • Platelet thrombi develop in areas of endothelial injury.
    3. Clinical findings
    a. Symptoms begin 24 to 72 hours after trauma.
    b. Restlessness, delirium, coma
    c. Dyspnea, tachypnea
    Fat microglobules in pulmonary capillaries cause hypoxemia.
    Massive perfusion defect
    d. Petechiae commonly develop over the chest and upper extremities.
    • Due to thrombocytopenia from platelet adhesion to microglobules of tat
    e. Death results in less than 10% of cases.
    4. Diagnosis
    a. Usually a clinical diagnosis based on above findings
    b. Search for fat globules in urine, pulmonary alveolar lavage, spinal fluid
    5. Treatment is supportive
    • Maintain good arterial oxygenation
  • Thrombosis
    • A thrombus is an intravascular mass attached to the vessel wall and is composed of varying proportions of coagulation factors, RBGs. and platelets.
    A, Pathogenesis of thrombi
    1. Endothelial cell injury
    • Due to turbulent blood flow at arterial bifurcations or overlying atherosclerotic plaques; cigarette smoke
    2. Stasis of blood flow
    • Sluggish blood flow due to prolonged bed rest or sitting (e.g.. long airplane flight)
    3. Hypercoagulahility
    a. Activation of coagulation system
    b. Causes of hypercoagulability
    1) Hereditary or acquired factor deficiencies
    • Example—hereditary antithrombin III deficiency or acquired deficiency due to oral contraceptives
    2) Antiphospholipid syndrome
    • Due to lupus anticoagulant and/or anticardiolipin antibodies
  • Types of thrombi
    1. Venous thrombi
    a. Pathogenesis
    1). Stasis
    (a) Procoagulants (e.g., tissue thromboplastin) released from damaged endothelium cause localized activation ofthen coagulation system.
    (b) Fibrin is produced, which forms a mesh around RBGs. platelets, and white blood cells in the stagnant blood within the vessel to produce a thrombus,
    2). Hypercoagulable state
    b. Sites
    (1) Deep vein in the lower extremity below the knee
    (2) Other sites
    • Superficial saphenous, hepatic, and renal veins; dural sinuses
    c. Composition
    (1) Adherent, occlusive, dark red fibrin clot
    • Contains entrapped RBCs (primary component), white blood cells, and platelets
    (2) In the lower extremities, they propagate (extend) toward the heart.
    • Danger of pulmonary artery embolization once they reach the femoral vein
    d. Anticoagulants heparin and warfarin prevent formation of venous thrombi.
    (1) Anticoagulants do not dissolve the thrombus: they only prevent further formation of a thrombus.
    (2) The fibrinolytic system (plasmin) is responsible for dissolution of the thrombus.
    Arterial thrombi
    a. Pathogenesis
    1) Endothelial cell injury due to turbulent blood flow
    • Platelets adhere to areas of injury.
    2) Hypercoagulable state
    b. Sites
    Elastic and muscular arteries
    Majority of thrombi overlie disrupted atherosclerotic plaques
    • Example—coronary artery thrombosis
    c. Composition of thrombi in muscular arteries and aortic branches
    1) Adherent, usually occlusive, gray-white fibrin clot composed of platelets
    2) Aspirin and other inhibitors of platelet aggregation prevent formation of these thrombi.
    d. Composition of thrombi in the heart chambers and aorta
    1) Laminated thrombi with alternating pale and red areas (lines of Zahn)
    (a) Pale areas are composed of platelets held together by fibrin.
    (b) Red areas are composed predominantly of RBCs held together by fibrin,
    (c) Mixed type of thrombus
    2) Examples of thrombi in the heart chambers
    (a) Thrombus in left ventricle due to a transmural myocardial infarction (mural thrombus)
    (b) Thrombus in left atrium in patients with mitral stenosis complicated by atrial fibrillation
    3) Thrombi in the aorta usually develop in aneurysms,
    • Example—abdominal aortic aneurysm
    4) Aspirin along with anticoagulant therapy helps to prevent these types of mixed thrombi.
    e. Clinical findings in arterial thrombosis
    1) Infarction (e.g.. acute myocardial infarction, stroke)
    2) Embolization
    3. Postmortem clot
    a. Fibrin clot of plasma (resembles chicken fat) without entrapped cells
    b. It is not attached to the vessel wall.
  • Typical disorders of peripheral blood flow

    1. 1. PPllaann ooff tthhee lleeccttuurree • DDiissoorrddeerrss ooff ppeerriipphheerraall bblloooodd ffllooww • MMiiccrroocciirrccuullaattiioonn • DDiissoorrddeerrss ooff llyymmpphhoocciirrccuullaattiioonn • EEddeemmaa • DDeeffiinniittiioonn ooff tthhee ccoonncceepptt ooff aarrtteerriiaall hhyyppeerreemmiiaa,, eettiioollooggyy aanndd ppaatthhooggeenneessiiss,, ccllaassssiiffiiccaattiioonn.. SSyymmppttoommss.. • EEttiioollooggyy aanndd ppaatthhooggeenneessiiss ooff vveennoouuss hhyyppeerreemmiiaa ((ccoonnggeessttiioonn)),, eettiioollooggyy aanndd ppaatthhooggeenneessiiss,, ssyymmppttoommss.. • DDeeffiinniittiioonn ooff tthhee ccoonncceepptt ooff iisscchheemmiiaa.. EEttiioollooggyy,, ppaatthhooggeenneessiiss ooff iisscchheemmiiaa,, ssyymmppttoommss.. • CCoonncceepptt ooff rreeppeerrffuussiioonn ssyynnddrroommee,, iisscchheemmiicc ttooxxiiccoossiiss.. • DDeeffiinniittiioonn ooff ssttaassiiss.. EEttiioollooggyy.. PPaatthhooggeenneessiiss.. CCaappiillllaarryy ((ttrruuee)) ssttaassiiss.. • EEmmbboolliissmm.. EEttiioollooggyy.. PPaatthhooggeenneessiiss.. • TThhrroommbboossiiss aass aa rreeaassoonn ooff ppeerriipphheerraall cciirrccuullaattiioonn ddiissoorrddeerr.. EEttiioollooggyy aanndd ppaatthhooggeenneessiiss..
    2. 2. AAccttuuaalliittyy ooff tthhee lleeccttuurree Blood vessels function in the delivery of oxygen and nutrients to the tissues and in the removal of waste products from the tissues. Unlike disorders of the respiratory system or central circulation that cause hypoxia and impair oxygenation of tissues throughout the body, the effects of blood vessel disease usually are limited to local tissues supplied by a particular vessel or group of vessels. Disturbances in blood flow can result from pathologic changes in the vessel wall (i.e., atherosclerosis, vasculities), acute vessel obstruction caused by thrombus or embolus, vasospasm (i.e., Raynaud’s phenomenon), abnormal vessel dilation (i.e., arterial aneurysms or varicose veins), or compression of blood vessels by extravascular forces (i.e., tumors, edema, or firm surfaces such as those associated with pressure ulcers).
    3. 3. DDiissoorrddeerrss ooff ppeerriipphheerraall bblloooodd ffllooww::  ssyysstteemmiicc ddiissoorrddeerrss,, wwhhiicchh ccoonnnneeccttiinngg wwiitthh iinnssuuffffiicciieennccyy ooff ccaarrddiioo--vvaassccuullaarr ssyysstteemm ((ddiissoorrddeerrss ooff ggeenneerraall hheemmooddyynnaammiicc))  ddiissoorrddeerrss ooff llooccaall ppeerriipphheerraall ffllooww –– iitt iiss ddiissoorrddeerrss cciirrccuullaattiioonn ooff tthhee bblloooodd iinn oorrggaannss aanndd ttiissssuueess..
    4. 4. • Local peripheral flow disorders distinguish on two groups in dependence on vessels size: • 11 – disorders of mmiiccrroocciirrccuullaattiioonn – the diameter of vessels is less 100 micrometer, • 22 – disorders of mmaaccrroocciirrccuullaattiioonn – the diameter of vessels is more 100 micrometer.
    5. 5. DDiissoorrddeerrss ooff mmiiccrroocciirrccuullaattiioonn 1) disorders of hheemmoommiiccrroocciirrccuullaattiioonn (in blood vessels) 22)) llyymmpphhcciirrccuullaattiioonn (in lymphatic vessels).
    6. 6. MMiiccrroocciirrccuullaattoorryy bbllooooddssttrreeaamm ccoonnssiissttss ooff:: • arterioles, • precapillaries, • precapillary sphincters, • capillaries, • postcapillaries, • venules, • small veins, • arteriovenular anastomoses, • lymphatic vessels.
    7. 7. RReeaassoonnss ooff ddiissoorrddeerrss ooff hheemmoommiiccrroocciirrccuullaattiioonn:: 11)) iinnttrraavvaassccuullaarr disorders 2) disorders of structure and function of vascular wall (ttrraannssmmuurraall), 3) extravascular disorders. Changes of viscosity and blood and lymph volume develop as a result of hemoconcentration and hemodilution.
    8. 8. IInnttrraavvaassccuullaarr ddiissoorrddeerrss  aaccccoommppaanniieedd bbyy aaggggrreeggaattiioonn ooff eerryytthhrrooccyytteess,, ppllaatteelleettss aanndd lleeuukkooccyytteess.. AAggggrreeggaattiioonn ooff ppllaatteelleettss.. EEttiioollooggyy.. CCaauusseess ooff aaggggrreeggaattiioonn ooff ppllaatteelleettss::  ­ ccoonncceennttrraattiioonn AADDPP ((aass rreessuulltt ddeessttrrooyyiinngg ooff cceellll)),,  ­ ccoonncceennttrraattiioonn ccaatteecchhoollaammiinneess ((ssttrreessss,, eemmoottiioonn)),,  aaccccuummuullaattiioonn iinn tthhee bblloooodd ffrreeee ffaattttyy aacciiddss,,  aaccttiivvaattiioonn ooff cceelllluullaarr pphhoosspphhoolliippaasseess,,  aaccttiivvaattiioonn ooff FFOOLL ((ffrreeee lliippiidd ooxxiiddaattiioonn)),,  ­ ccoonncceennttrraattiioonn FFAAPP ((ffaaccttoorr ooff aaccttiivvaattiioonn ppllaatteelleettss)),,  aacciiddoossiiss,, eettcc..
    9. 9.  PPaatthhooggeenneessiiss.. AAnnyy ccaauussee →→ lleeaadd ttoo aaccttiivvaattiioonn ooff mmeemmbbrraannee pphhoosspphhoolliippaassee AA22 →→ hhyyddrroollyyssiiss ooff pphhoosspphhoolliippiiddss ooff ppllaatteelleettss mmeemmbbrraanneess aanndd aappppeennddiixxeess aarree ffoorrmmeedd oonn mmeemmbbrraannee →→ ccoonnttaaccttiinngg ttwwoo cceellllss bbyy tthheessee aappppeennddiixxeess →→ aaggggrreeggaattiioonn ooff ppllaatteelleettss..
    10. 10. AAggggrreeggaattiioonn ooff RRBBCC EEttiioollooggyy..  ¯ aammoouunntt ooff aallbbuummiinnss iinn tthhee bblloooodd,,  ­ aammoouunntt ooff gglloobbuulliinnss,,  ­ ccoonncceennttrraattiioonn ffiibbrriinnooggeennss aanndd ffiibbrriinnss iinn tthhee bblloooodd,,  ­ ccoonncceennttrraattiioonn ooff HH++((hhyyddrrooggeenn)) iioonnss →→ aacciiddoossiiss,,  ­ ccoonncceennttrraattiioonn AADDPP ((aass rreessuulltt ddeessttrrooyyiinngg ooff cceellll)),,  aaccccuummuullaattiioonn iinn tthhee bblloooodd ffrreeee ffaattttyy aacciiddss,,  aaccttiivvaattiioonn ooff FFOOLL,, eettcc..
    11. 11. SSlluuddggee  SSlluuddggee iiss aa pphheennoommeennoonn cchhaarraacctteerriizzeedd bbyy aaddhheessiioonn,, aaggggrreeggaattiioonn aanndd aagggglluuttiinnaattiioonn ooff bblloooodd cceellllss wwhhiicchh ccaauusseess bblloooodd ttoo ddiissiinntteeggrraattee iinnttoo ccoonngglloommeerraatteess ooff eerryytthhrrooccyytteess,, lleeuukkooccyytteess,, tthhrroommbbooccyytteess aanndd ppllaassmmaa aanndd iinndduucceess mmiiccrroocciirrccuullaattiioonn ddiissttuurrbbaanncceess.. PPaatthhooggeenneessiiss.. AAnnyy ccaauussee lleeaadd ttoo cchhaannggee mmeemmbbrraannee cchhaarrggee ffrroomm nneeggaattiivvee ttoo ppoossiittiivvee oonn eerryytthhrrooccyytteess,, aanndd oonn eennddootthheelliiuumm vviiccee vveerrssaa.. IItt iiss ccaauusseedd ttoo eelleeccttrroossttaattiicc rreellaattiioonnsshhiipp ooff tthheessee cceellllss aanndd aaggggrreeggaattiioonn ooff tthheemm.. MMaayy bbee ffoorrmmeedd sslluuddggee ooff eerryytthhrrooccyytteess:: • ccllaassssiiccaall ((mmoorree tthhaann 110000 eerryytthhrrooccyytteess)),, • ddeexxttrriinn • aammoorrpphhoouuss ((33--44 eerryytthhrrooccyytteess))..
    12. 12. AAggggrreeggaattiioonn ooff lleeuukkooccyytteess EEttiioollooggyy.. CCaauusseess aarree ssiimmiillaarr ttoo ccaauusseess ooff aaggggrreeggaattiioonn ooff eerryytthhrrooccyytteess aanndd ppllaatteelleettss,, pplluuss mmoosstt ssttrroonngg ffaaccttoorr –– mmiiccrroooorrggaanniissmmss aanndd tthheeiirrss ttooxxiinnss.. PPaatthhooggeenneessiiss.. AAnnyy ccaauussee →→ aaccttiivvaattiioonn ooff pphhoosspphhoolliippaassee AA22 →→ hhyyddrroollyyssiiss ooff pphhoosspphhoolliippiiddss ooff lleeuukkooccyytteess →→ pprroodduuccttiioonn aarraacchhiiddoonniicc aacciidd →→ ccrreeaattiioonn tthhee lleeuukkoottrriieenneess uunnddeerr tthhee aaccttiioonn ooff lliippooxxyyggeennaassee.. CCoonncclluussiioonn:: aaggggrreeggaattiioonn ooff bblloooodd cceellllss ccaauusseess ttoo nnaarrrroowwiinngg ooff lluummeenn ooff vveesssseellss oorr tthheeiirr oocccclluussiioonn..
    13. 13. Disorders ooff ssttrruuccttuurree aanndd ffuunnccttiioonn ooff vvaassccuullaarr wwaallll (TTrraannssmmuurraall)  related with edema and destroying components of vascular structure: endothelium cells, basement membrane, connective tissue.  It leads to narrowing of lumen of vessels or their occlusion, disorders of hematocellular barriers → damage of cells, trophic disturbances.
    14. 14. Transmural ddiissttuurrbbaanncceess aarree ssuubbddiivviiddeedd iinnttoo ttwwoo ccaatteeggoorriieess:: 11)) ppeerrmmeeaabbiilliittyy ddiissttuurrbbaanncceess 22)) eemmiiggrraattiioonn ddiissttuurrbbaanncceess.. IInnccrreeaasseedd ppeerrmmeeaabbiilliittyy ooff mmiiccrroovvaassccuullaarr wwaallllss aaccttiivvaatteess tthhee mmeecchhaanniissmmss ooff fflluuiidd ttrraannssffeerr::  ffiillttrraattiioonn ((fflluuiidd ttrraannssppoorrtt aaccccoorrddiinngg ttoo hhyyddrroossttaattiicc pprreessssuurree ggrraaddiieenntt));;  ddiiffffuussiioonn ((fflluuiidd ttrraannssppoorrtt wwhhiicchh ddooeess nnoott iinnvvoollvvee aannyy eenneerrggyy lloosssseess));;  oossmmoossiiss ddiirreecctteedd fflluuiidd ddiiffffuussiioonn aaccccoorrddiinngg ttoo oossmmoottiicc pprreessssuurree ggrraaddiieenntt)).. DDeeccrreeaasseedd ppeerrmmeeaabbiilliittyy  CCaauusseess:: tthhiicckkeenniinngg aanndd//oorr iinndduurraattiioonn ooff tthhee vvaassccuullaarr wwaallllss,, oorr ddiissttuurrbbaanncceess ooff eenneerrggyy ssuuppppllyy ooff iinnttrraacceelllluullaarr pprroocceesssseess..  CCoonnsseeqquueenncceess.. DDeeccrreeaasseedd eeffffiicciieennccyy ooff fflluuiidd ttrraannssffeerr mmeecchhaanniissmmss:: ffiillttrraattiioonn,, ddiiffffuussiioonn,, ttrraannssccyyttoossiiss,, oossmmoossiiss..
    15. 15. EExxttrraavvaassccuullaarr ddiissttuurrbbaanncceess ooff  IInnccrreeaasseedd oorr ddeeccrreeaasseedd mmiiccrroocciirrccuullaattiioonn vvoolluummee ooff iinnttrraacceelllluullaarr fflluuiidd wwhhiicchh rreessuullttss iinn iittss sslloowweerr ffllooww iinnttoo mmiiccrroocciirrccuullaattoorryy vveesssseellss  EExxttrraacceelllluullaarr ddiissoorrddeerrss aarree ccaauusseedd bbyy ssttrruuccttuurraall aanndd ffuunnccttiioonnaall cchhaannggeess ooff ccoommppoonneennttss ooff ccoonnnneeccttiivvee ttiissssuuee ssuurrrroouunndd tthhee vveesssseellss..  TThhee mmaaiinn rroollee ooff tthhiiss ddiissoorrddeerrss ppllaayyeedd ttiissssuuee bbaassoopphhiilleess ((mmaasstt cceellllss)) aanndd tthheeiirr ddeeggrraannuullaattiioonn.. IItt hhaass ssoommee ggrraannuulleess ooff bbiioollooggiiccaall aaccttiivviittyy ssuubbssttaanncceess:: hhiissttaammiinnee,, hheeppaarriinn aanndd sseerroottoonniinn..  CCaauusseess ooff ddeeggrraannuullaattiioonn:: AADDPP,, LLTT BB44,, ccoommpplleexx aannttiiggeenn--aannttiibbooddyy,, pprroodduuccttss ooff aaccttiivvaattiinngg ccoommpplleemmeennttss,, mmeecchhaanniiccaall ttrraauummaa,, eettcc..
    16. 16. EEffffeeccttss ooff hhiissttaammiinnee:: • 11)) iinnccrreeaassee aa ppeerrmmeeaabbiilliittyy ooff vvaassccuullaarr wwaallll ((eeddeemmaa aanndd ccoonnttrraaccttiioonn ooff eennddootthheelliiuumm cceellll)) →→ iinnccrreeaassee eexxttrraavvaassccuullaarr oonnccoottiicc pprreessssuurree,, • 22)) eeddeemmaa,, • 33)) ppaaiinn oorr iittcchh –– ccaauusseedd bbyy iirrrriittaattiioonn ooff nneerrvvoouuss rreecceeppttoorrss bbyy hhiissttaammiinnee,, • 44)) ddiillaattaattiioonn oorr ccoonnssttrriiccttiioonn bblloooodd vveesssseellss –– HH22 ((hhiissttaammiinnee)) oorr HH11-- rreecceeppttoorrss aaccccoorrddiinnggllyy ((ccoorrrreessppoonnddiinnggllyy,, ccoonnffoorrmmaabbllyy,, ssuuiittaabbllyy))..
    17. 17.  SSeerroottoonniinn hhaass ssiimmiillaarr eeffffeeccttss ++ iitt lleeaadd ttoo vveennuulleess ccoonnssttrriiccttiioonn,, tthhaatt iinnccrreeaassee tthhee hhyyddrroossttaattiicc pprreessssuurree ((hhyyddrroossttaattiicc llooaadd)) iinn ccaappiillllaarriieess..  HHeeppaarriinnee ––aannttiiccooaagguullaattiivvee aaccttiioonn →→ mmaayy bbee aa ccaauussee ooff bblleeeeddiinngg ((hhaaeemmoorrrrhhaaggee))..  EExxppoosseedd ccoollllaaggeenn ooff bbaassiicc mmeemmbbrraannee ooff vvaassccuullaarr wwaallll iiss iinniittiiaattoorr ooff aaddhheessiioonn aanndd aaggggrreeggaattiioonn ooff ppllaatteelleettss..
    18. 18. DDiissoorrddeerrss ooff llyymmpphhcciirrccuullaattiioonn  IItt iiss aa ttyyppiiccaall ppaatthhoollooggiiccaall pprroocceessss,, wwhhaatt cchhaarraacctteerriizzeedd bbyy aaccccuummuullaattiioonn ooff llyymmpphh iinn ttiissssuueess aanndd ddeevveellooppmmeenntt ooff llyymmpphhaattiicc eeddeemmaa ((eelleepphhaannttiiaassiiss)).. PPaatthhooggeenneessiiss.. MMeecchhaanniissmmss ooff ddiissoorrddeerrss ooff llyymmpphhcciirrccuullaattiioonn:: 11)) mmeecchhaanniiccaall –– rreellaatteedd ttoo ccoommpprreessssiioonn ooff llyymmpphhaattiicc vveesssseellss ((bbyy ttuummoorrss,, ssccaarrss,, eeddeemmaa)) aanndd tthheeiirr oobbssttrruuccttiioonn ((bbyy ttuummoorrss cceellllss,, bbaacctteerriiaa''ss,, ffoorreeiiggnn bbooddyy)).. 22)) aakkiinneettiicc ((hhyyppookkiinneettiicc)) ccaauusseedd wwiitthh ddeeccrreeaassee ccoonnssttrriiccttiioonn pprrooppeerrttyy ooff llyymmpphhaattiicc vveesssseellss.. WWee hhaavvee tthhiiss oonn ddiissoorrddeerrss ooff ddiiaapphhrraaggmmss oorr ddiissoorrddeerrss ooff ssuuccttiioonn aaccttiioonn ooff tthhoorraaxx.. 33)) ddyynnaammiiccaall ccaauusseedd bbyy eexxcceessssiivvee pprroodduuccttiioonn ooff iinntteerrcceelllluullaarr lliiqquuiiddss ((ddiisseeaasseess ooff hheeaarrtt,, kkiiddnneeyyss)).. 44)) rreessoorrppttiivvee mmeecchhaanniissmm –– iitt iiss ddiissoorrddeerrss ooff ddrraaiinnaaggee ffuunnccttiioonn ooff llyymmpphhaattiicc vveesssseellss,, iinn tthhee pprreesseennccee ooff nnoorrmmaall aammoouunntt ooff llyymmpphh.. IItt ccaauusseess bbyy iinnccrreeaassee ooff ccoollllooiidd--oossmmoottiicc pprreessssuurree ooff iinntteerrcceelllluullaarr lliiqquuiiddss ((iinnffllaammmmaattiioonn,, aalllleerrggyy))..
    19. 19. EElleepphhaannttiiaassiiss IImmppaaiirreedd llyymmpphhaattiicc ddrraaiinnaaggee aanndd ccoonnsseeqquueenntt llyymmpphheeddeemmaa iiss uussuuaallllyy llooccaalliizzeedd;; iitt ccaann rreessuulltt ffrroomm iinnffllaammmmaattoorryy oorr nneeooppllaassttiicc oobbssttrruuccttiioonn.. FFoorr eexxaammppllee,, tthhee ppaarraassiittiicc iinnffeeccttiioonn ffiillaarriiaassiiss ccaann ccaauussee eexxtteennssiivvee iinngguuiinnaall llyymmpphhaattiicc aanndd llyymmpphh nnooddee ffiibbrroossiiss.. TThhee rreessuullttaanntt eeddeemmaa ooff tthhee eexxtteerrnnaall ggeenniittaalliiaa aanndd lloowweerr lliimmbbss ccaann bbee ssoo mmaassssiivvee aass ttoo eeaarrnn tthhee aappppeellllaattiioonn eelleepphhaannttiiaassiiss.. LLyymmpphheeddeemmaa aa.. PPrrootteeiinn--rriicchh fflluuiidd bb.. NNoonn--ppiittttiinngg eeddeemmaa
    20. 20.  TThhee tteerrmm eeddeemmaa ssiiggnniiffiieess iinnccrreeaasseedd fflluuiidd iinn tthhee iinntteerrssttiittiiaall ttiissssuuee ssppaacceess;  fflluuiidd ccoolllleeccttiioonnss iinn ddiiffffeerreenntt bbooddyy ccaavviittiieess aarree vvaarriioouussllyy ddeessiiggnnaatteedd :: hhyyddrrootthhoorraaxx hhyyddrrooppeerriiccaarrddiiuumm HHyyddrrooppeerriittoonneeuumm ((aasscciitteess))  AAnnaassaarrccaa iiss aa sseevveerree aanndd ggeenneerraalliizzeedd eeddeemmaa wwiitthh pprrooffoouunndd ssuubbccuuttaanneeoouuss ttiissssuuee sswweelllliinngg..
    21. 21. IInnccrreeaasseedd hhyyddrroossttaattiicc pprreessssuurree,, ccaauusseedd bbyy aa rreedduuccttiioonn iinn vveennoouuss rreettuurrnn ((aass iinn hheeaarrtt ffaaiilluurree)).. DDeeccrreeaasseedd ccoollllooiidd oossmmoottiicc pprreessssuurree,, ccaauusseedd bbyy rreedduucceedd ccoonncceennttrraattiioonn ooff ppllaassmmaa aallbbuummiinn ((dduuee ttoo ☼ ddeeccrreeaasseedd ssyynntthheessiiss,, aass iinn lliivveerr ddiisseeaassee,, ☼ iinnccrreeaasseedd lloossss,, aass iinn kkiiddnneeyy ddiisseeaassee)).. LLyymmpphhaattiicc oobbssttrruuccttiioonn tthhaatt iimmppaaiirrss iinntteerrssttiittiiaall fflluuiidd cclleeaarraannccee ((aass iinn ssccaarrrriinngg,, ttuummoorrss,, oorr cceerrttaaiinn iinnffeeccttiioonnss)).. PPrriimmaarryy rreennaall ssooddiiuumm rreetteennttiioonn ((iinn rreennaall ffaaiilluurree)).. IInnccrreeaasseedd vvaassccuullaarr ppeerrmmeeaabbiilliittyy ((iinn iinnffllaammmmaattiioonn))
    22. 22. Pathophysiologic CCaatteeggoorriieess ooff EEddeemmaa IInnccrreeaasseedd HHyyddrroossttaattiicc PPrreessssuurree IImmppaaiirreedd vveennoouuss rreettuurrnn •CCoonnggeessttiivvee hheeaarrtt ffaaiilluurree •CCoonnssttrriiccttiivvee ppeerriiccaarrddiittiiss •AAsscciitteess ((lliivveerr cciirrrrhhoossiiss)) •VVeennoouuss oobbssttrruuccttiioonn oorr ccoommpprreessssiioonn ☼ TThhrroommbboossiiss ☼ EExxtteerrnnaall pprreessssuurree ((ee..gg..,, mmaassss)) ☼ LLoowweerr eexxttrreemmiittyy iinnaaccttiivviittyy wwiitthh pprroolloonnggeedd ddeeppeennddeennccyy AArrtteerriioollaarr ddiillaattiioonn • HHeeaatt • NNeeuurroohhuummoorraall ddyyssrreegguullaattiioonn RReedduucceedd PPllaassmmaa OOssmmoottiicc PPrreessssuurree ((HHyyppoopprrootteeiinneemmiiaa)) •PPrrootteeiinn--lloossiinngg gglloommeerruullooppaatthhiieess ((nneepphhrroottiicc ssyynnddrroommee)) •LLiivveerr cciirrrrhhoossiiss ((aasscciitteess)) •MMaallnnuuttrriittiioonn •PPrrootteeiinn--lloossiinngg ggaassttrrooeenntteerrooppaatthhyy LLyymmpphhaattiicc OObbssttrruuccttiioonn •IInnffllaammmmaattoorryy •NNeeooppllaassttiicc •PPoossttssuurrggiiccaall •PPoossttiirrrraaddiiaattiioonn SSooddiiuumm RReetteennttiioonn EExxcceessssiivvee ssaalltt iinnttaakkee wwiitthh rreennaall iinnssuuffffiicciieennccyy IInnccrreeaasseedd ttuubbuullaarr rreeaabbssoorrppttiioonn ooff ssooddiiuumm ☼ RReennaall hhyyppooppeerrffuussiioonn ☼ IInnccrreeaasseedd rreenniinn-- aannggiiootteennssiinn--aallddoosstteerroonnee sseeccrreettiioonn IInnffllaammmmaattiioonn •AAccuuttee iinnffllaammmmaattiioonn •CChhrroonniicc iinnffllaammmmaattiioonn •AAnnggiiooggeenneessiiss
    23. 23. FFaaccttoorrss aaffffeeccttiinngg fflluuiidd bbaallaannccee aaccrroossss ccaappiillllaarryy wwaallllss • Capillary hydrostatic and osmotic forces are normally balanced so that there is no net loss or gain of fluid across the capillary bed. • However, increased hydrostatic pressure or diminished plasma osmotic pressure leads to a net accumulation of eexxttrraavvaassccuullaarr fflluuiidd ((eeddeemmaa)).. • As the interstitial fluid pressure increases, tissue lymphatics remove much of the excess volume, eventually returning it to the circulation via the thoracic duct. • If the ability of the lymphatics to drain tissue is exceeded, persistent tissue edema results.
    24. 24.  NNoonn--ppiittttiinngg eeddeemmaa::  iiss oofftteenn rreeffeerrrreedd ttoo aass llyymmpphheeddeemmaa wwhhiicchh iiss aa ddiissttuurrbbaannccee ooff tthhee llyymmpphhaattiicc ssyysstteemm;;  ccaann ddeevveelloopp aafftteerr ssyysstteemmiicc ttiissssuuee ssuucchh aass aafftteerr aa mmaasstteeccttoommyy;;  ddooeess nnoott rreessppoonndd ttoo ddiiuurreettiiccss  pprrootteeiinn--rriicchh fflluuiidd..  PPiittttiinngg eeddeemmaa::  IIss tthhee ccllaassssiiccaall,, mmoosstt ccoommmmoonn ttyyppee oobbsseerrvveedd iinn cclliinniicc;;  GGeenneerraallllyy rreessppoonnddss ttoo ddiiuurreettiicc tthheerraappyy;;  CCoommmmoonn ccaauusseess iinncclluuddee nneepphhrroottiicc ssyynnddrroommee,, ccoonnggeessttiivvee hheeaarrtt ffaaiilluurree ((rriigghhtt ssiiddee HHFF dduuee ttoo  hhyyddrroossttaattiicc pprreessssuurree)),, cciirrrrhhoossiiss ((dduuee ttoo  oonnccoottiicc pprreessssuurree)),, pprreeggnnaannccyy,, iiddiiooppaatthhiicc aanndd nnuuttrriittiioonnaall eeddeemmaa.. GGllyyccoossaammiinnooggllyyccaannss aa..  iinn hhyyaalluurroonniicc aacciidd aanndd cchhoonnddrrooiittiinn ssuullffaattee bb.. NNoonn--ppiittttiinngg eeddeemmaa ccaalllleedd mmyyxxeeddeemmaa
    25. 25. AAppppllyyiinngg pprreessssuurree ttoo tthhee sswwoolllleenn aarreeaa ccaauusseess aann iinnddeennttaattiioonn tthhaatt pprreesseennttss ffoorr ssoommee ttiimmee
    26. 26. DDiissoorrddeerrss ooff mmaaccrroocciirrccuullaattiioonn " ­ 100 mcm • There are 6 types: 1. Arterial hyperemia. 2. Venous hyperemia. 3. Ischemia. 4. Stasis. 5. Thrombosis. 6. Embolism.
    27. 27. AArrtteerriiaall ((aaccttiivvee)) hhyyppeerreemmiiaa Arterial hyperemia – pathological or physiological states, which are characterized by llooccaall iinnccrreeaassiinngg ooff bblloooodd iinnffllooww from arterial vessels to microcirculation.
    28. 28. o The causes off aarrtteerriiaall hhyyppeerreemmiiaass ccaann bbee ooff vvaarriioouuss eettiioollooggyy aanndd nnaattuurree ► OOrriiggiinn rreessuullttiinngg ffrroomm eennddooggeennoouuss aanndd eexxooggeennoouuss aaggeennttss.. ► EExxooggeennoouuss aaggeennttss:: IInnffeeccttiioouuss ((mmiiccrroooorrggaanniissmmss aanndd//oorr tthheeiirr eennddoo-- aanndd eexxoottooxxiinnss)) NNoonniinnffeeccttiioouuss ffaaccttoorrss ooff vvaarriioouuss nnaattuurree ► EEnnddooggeennoouuss ffaaccttoorrss,, rreessuullttiinngg iinn aarrtteerriiaall hhyyppeerreemmiiaa ffoorrmm iinn tthhee oorrggaanniissmmss:: 11)) ssaalltt aanndd ccoonnccrreemmeenntt ddeeppoossiittss iinn tthhee ttiissssuueess ooff kkiiddnneeyyss,, lliivveerr,, ssuubbccuuttaanneeoouuss ffaatt;; 22)) ffoorrmmaattiioonn ooff BBAASS ccaauussiinngg tthhee rreedduuccttiioonn ooff tthhee ttoonnee ooff ssmmooootthh mmuussccllee ooff aarrtteerriioolleess ((vvaassooddiillaattaattiioonn)),, aaddeennoossiinnee,, pprroossttaaggllaannddiinn,, kkiinniinneess;; 33)) aaccccuummuullaattiioonn ooff oorrggaanniicc aacciiddss ((llaaccttiicc,, ppyyrruuvviicc,, kkeettoogglluuttaarriicc))..
    29. 29. • BByy eettiioollooggiiccaall aaggeenntt:: 1) 2) 3) mmeecchhaanniiccaall eexxppoossuurree vveerryy hhiigghh tt00 eelleeccttrriicc ccuurrrreenntt PPhhyyssiiccaall aaggeenntt BBiioollooggiiccaall aaggeenntt oorrggaanniicc aanndd iinnoorrggaanniicc aacciiddss aallkkaallii aallddeehhyyddeess aallccoohhooll aacceettyyllcchhoolliinnee aaddeennoossiinnee nniittrrooggeenn ooxxiiddee pphhyyssiioollooggiiccaallllyy aaccttiivvee ssuubbssttaanncceess ffoorrmmiinngg iinn tthhee bbooddyy CChheemmiiccaall aaggeenntt
    30. 30. CCllaassssiiffiiccaattiioonn aanndd mmeecchhaanniissmmss I. PPhhyyssiioollooggiiccaall aarrtteerriiaall hhyyppeerreemmiiaa:: • 11)) wwoorrkkiinngg –– oorrggaann hhyyppeerrffuunnccttiioonn ((mmuussccllee,, iinntteessttiinnee,, eettcc)) • 22)) eemmoottiioonnaall ((ppssyycchhooggeenniicc)) –– iittss ccoonnddiittiioonnaall rreefflleexx ((sshhaammee,, eexxcciitteemmeenntt,, ccoonnffuussiioonn)) • 33)) rreeaaccttiivvee ((ssuubbssttiittuuttee)) –– hhyyppeerreemmiiaa aafftteerr sshhoorrtt--tteerrmm ((ttrraannssiittoorryy)) iisscchheemmiiaa.. IIII.. PPaatthhoollooggiiccaall aarrtteerriiaall hhyyppeerreemmiiaa:: • 11)) nneeuurrooggeenniicc ((nneeuurrooggeennoouuss)):: - aa)) nneeuurroottoonniicc - bb)) nneeuurrooppaarraallyyttiicc • 22)) mmeettaabboolliicc..
    31. 31. NNeeuurroottoonniicc aarrtteerriiaall hhyyppeerreemmiiaa Are ccaauusseedd bbyy ssttiimmuullaattiioonn ooff:: β-adrenorecetors, M-cholinoreceptors, H2-histaminoreceptors, activation of parasympathetic nervous system, irritation of vascular-dilatators part of vascular center or inhibition of vascular-constrictor part of this center. • IItt iiss cchhaarraacctteerriizzeedd bbyy pprreeddoommiinnaannccee ooff tthhee ppaarraassyymmppaatthheettiicc nneerrvvoouuss ssyysstteemm eeffffeeccttss ((iinn ccoommppaarriissoonn wwiitthh tthhee ssyymmppaatthheettiicc oonnee)) oonn aarrtteerriiaall vvaassccuullaarr wwaallllss..
    32. 32. Neuroparalytic arterial hyperemia • Are caused by damage or blockage of α-adrenoreceptors sympathetic nervous system. • As usual tone of vessels is supplied by the impulses from ssyymmppaatthheettiicc nneerrvveess (1-3 impulses for a second) to smooth muscle cell of vascular wall. • IItt iiss cchhaarraacctteerriizzeedd bbyy rreedduuccttiioonn oorr aabbsseennccee ((ppaarraallyyssiiss)) ooff tthhee ssyymmppaatthheettiicc nneerrvvoouuss ssyysstteemm eeffffeeccttss oonn tthhee wwaallllss ooff tthhee aarrtteerriieess aanndd aarrtteerriioolleess..
    33. 33. EExxaammpplleess:: -- PPaatthhoollooggiiccaall aarrtteerriiaall hhyyppeerreemmiiaa ooff tthhee bbrraaiinn iinn hhyyppeerrtteennssiivvee ccrriissiiss.. -- AAccccoorrddiinngg ttoo tthhee nneeuurroommyyooppaarraallyyttiicc mmeecchhaanniissmm::  iinn tthhee oorrggaannss ooff tthhee aabbddoommiinnaall ccaavviittyy aafftteerr aasscciitteess,,  iinn tthhee sskkiinn aanndd mmuusscclleess aafftteerr aa ttiigghhtt ttoouurrnniiqquueett iiss rreemmoovveedd;;  aatt tthhee ssiittee ooff cchhrroonniicc iinnffllaammmmaattiioonn;;  aatt tthhee ssiittee wwhhiicchh wwaass eexxppoosseedd ttoo hheeaatt ffoorr ssoommee hhoouurrss ((ssuunn hheeaatt,, hhoott--wwaatteerr bboottttllee;; mmuussttaarrdd ppllaasstteerr aapppplliiccaattiioonn));;  iinn tthhee aarreeaa ooff ssyymmppaatthheettiicc ddeenneerrvvaattiioonn..
    34. 34. Appears under the action different chemical factors, which cause microparalysis of vessels independently from nervous influences. 11)) iinnoorrggaanniicc ssuubbssttaanncceess ((iinnccrreeaassee aa ccoonncceennttrraattiioonn ooff ppoottaassssiiuumm,, hhyyddrrooggeenn,, ccaarrbboonn ddiiooxxiiddee,, ddeeccrreeaassee tthhee NNOO--ffaaccttoorrss)) 2) metabolic substances (prostaglandins, kinines, histamine, ADP), 3) substances from necrotic places. • HHuummoorraall mmeecchhaanniissmm. It is characterized by a locally increased content of vasodilators – biologically active substances having a vasodilatating effect (adenosine, NO, PgE, kinines) and by increased sensitivity of receptors of arterial vascular walls to vasodilators. • Metabolic and oxygen supply disorders may cause hypertrophy and hyperplasia.
    35. 35. TThhee eeffffeeccttss ooff aarrtteerriiaall hhyyppeerreemmiiaa aarree:: ¨ tthhee iinnccrreeaassee ooff bblloooodd ffllooww ssppeeeedd,, ¨ tthhee iinnccrreeaassee ooff ffuunnccttiioonniinngg ccaappiillllaarriieess aammoouunntt,, ¨ tthhee rriissee ooff bblloooodd pprreessssuurree,, ssttrreennggtthheennss ooff tthhee ttiissssuueess ooxxyyggeennaattiioonn.. • AArrtteerriiaall hhyyppeerreemmiiaa pprroommootteess:: ¨ tthhee ddeerriivvaattiioonn ooff tthhee ooxxyyggeenn rraaddiiccaallss ffoorr tthhee pprrootteeccttiioonn ooff tthhee oorrggaanniissmm aaggaaiinnsstt tthhee mmiiccrroooorrggaanniissmmss,, ¨ ffoorrmmiinngg ooff hhuummoorraall ppllaassmmaa ffaaccttoorrss ooff tthhee oorrggaanniissmm pprrootteeccttiioonn ((ccoommpplleemmeenntt,, pprrooppeerrddiinnee,, ffiibbrroonneeccttiinnee)),, ¨ ccaauusseess tthhee mmoovveemmeenntt ooff lleeuuccooccyytteess iinnttoo tthhee aarreeaa ooff iinnjjuurryy.. AArrtteerriiaall hhyyppeerreemmiiaa ccaauusseess tthhee rreeddnneessss aanndd wwaarrmmtthh ooff tthhee iinnjjuurriioouuss aarreeaa ((hhiigghheerr mmeettaabboolliicc iinntteennssiittyy))..
    36. 36. VVeennoouuss hhyyppeerreemmiiaa VVeennoouuss hhyyppeerreemmiiaa –– llooccaall oorr ssyysstteemmiicc ddeeccrreeaassiinngg ooff bblloooodd oouuttffllooww ffrroomm mmiiccrroocciirrccuullaattiioonn.. CCaauusseess:: iinnttrraavvaassccuullaarr ffaaccttoorrss –– tthhrroommbboossiiss,, eemmbboolliissmm,, ffoorreeiiggnn bbooddiieess eettcc.. eexxttrraavvaassccuullaarr ffaaccttoorrss –– ccoommpprreessssiioonn tthhee vveesssseellss bbyy ttuummoorrss,, ssccaarrss,, eennllaarrggeemmeenntt oorrggaannss ((uutteerruuss wwiitthh ffeettuuss)).. ccoonnggeenniittaall ((iinnnnaattee)) aanndd aaccqquuiirreedd ddeeffeeccttss ooff ssttrruuccttuurree ooff vvaassccuullaarr wwaallll ooff vveennuueess ((ccoonnnneeccttiivvee aanndd mmuussccuullaarr ttiissssuueess)).. ggeenneerraalliizzeedd ddiissoorrddeerrss ooff bblloooodd ffllooww ccoonnnneecctt wwiitthh hheeaarrtt ffaaiilluurree.. CCoonnsseeqquueenncceess:: ddyyssttrroopphhiicc cchhaannggeess,, aattrroopphhyy,, eexxcceessssiivvee ggrroowwtthh ooff tthhee ccoonnnneeccttiivvee ttiissssuuee,, cciirrrrhhoossiiss,, pphhlleebboosscclleerroossiiss..
    37. 37. FFeeaattuurreess:: uunnddeerr mmiiccrroossccooppee:: iinnccrreeaassee ooff lluummeenn ccaappiillllaarriieess,, ppoossttccaappiillllaarriieess,, vveennuulleess;; bblloooodd ffllooww ssppeeeedd ddeeccrreeaassee,, ddiiaappeeddeessiiss ((ddiiaappiirreessiiss,, mmiiggrraattiioonn)).. PPhhyyssiioollooggiiccaall aanndd cclliinniiccaall ssiinnggss:: • eeddeemmaa,, • ccyyaannoossiiss,, • eennllaarrggeemmeenntt aanndd ddeeccrreeaassee tteemmppeerraattuurree ooff tthhee oorrggaann,, • iinnhhiibbiittiioonn ooff mmeettaabboolliicc pprroocceesssseess,, • ddeeccrreeaassee ooff ttiissssuuee ttuurrggoorr..
    38. 38. PPaatthhooggeenneettiicc eeffffeeccttss ooff vveennoouuss hhyyppeerreemmiiaa TThhee mmaajjoorr ppaatthhooggeenniicc ffaaccttoorrss aarree:: • HHyyppooxxiiaa ((ooff cciirrccuullaattoorryy ttyyppee aatt tthhee iinniittiiaall ssttaaggee ooff tthhee pprroocceessss aanndd ooff mmiixxeedd ttyyppee wwhheenn tthhee pprroocceessss iiss lloonngg-- tteerrmm)),, • TTiissssuuee eeddeemmaa ((rreessuullttiinngg ffrroomm iinnccrreeaasseedd hheemmooddyynnaammiicc pprreessssuurree oonn tthhee wwaallll ooff vveennuulleess aanndd vveeiinnss)).. • TTiissssuuee hheemmaattoommaass ((rreessuullttiinngg ffrroomm oovveerrddiisstteennssiioonn aanndd rruuppttuurree ooff ppoossttccaappiillllaarryy aanndd vveennuullaarr wwaallllss)) aanndd hheemmoorrhhaaggeess ((eexxtteerrnnaall aanndd iinntteerrnnaall)).. • CCoonnsseeqquueenncceess:: rreedduuccttiioonn ooff ssppeecciiffiicc aanndd nnoonn--ssppeecciiffiicc ffuunnccttiioonnss ooff oorrggaannss aanndd ttiissssuueess,, hhyyppoottrroopphhyy aanndd hhyyppooppllaassiiaa ooff ssttrruuccttuurraall eelleemmeennttss iinn ttiissssuueess aanndd oorrggaannss,, nneeccrroossiiss ooff ppaarreenncchhyymmaattoouuss cceellllss aanndd ccoonnnneeccttiivvee ttiissssuuee ddeevveellooppmmeenntt ((sscclleerroossiiss,, cciirrrrhhoossiiss)) iinn oorrggaannss..
    39. 39. IIsscchheemmiiaa  IIsscchheemmiiaa –– iiss aann iimmbbaallaannccee bbeettwweeeenn tthhee ssuuppppllyy ooff ttiissssuueess wwiitthh aarrtteerriiaall bblloooodd ffllooww aanndd tthheeiirr nneeeedd iinn iitt.. TThhee nneeeedd iinn bblloooodd ssuuppppllyy aallwwaayyss eexxcceeeeddss aaccttuuaall aammoouunntt ooff bblloooodd fflloowwiinngg tthhrroouugghh aarrtteerriieess.. EEttiioollooggyy  AAccccoorrddiinngg ttoo iittss nnaattuurree:: 11)) PPhhyyssiiccaall ffaaccttoorrss aarree ccoommpprreessssiioonn ooff aarrtteerriiaall vveesssseellss ((ee..gg.. bbyy ttuummoorrss,, ssccaarr ttiissssuuee,, ffoorreeiiggnn bbooddiieess,, ttoouurrnniiqquueettss)),, nnaarrrroowwiinngg oorr bblloocckkiinngg ooff aa lluummeenn ffrroomm iinnssiiddee ((ee..gg.. bbyy aa tthhrroommbbuuss,, eemmbboolluuss,, aatthheerroosscclleerroottiicc ppllaaqquuee)),, eexxppoossuurree ttoo eexxttrreemmeellyy ccoolldd tteemmppeerraattuurreess.. 22)) CChheemmiiccaall ffaaccttoorrss.. MMaannyy cchheemmiiccaall ccoommppoouunnddss ccaann ssttiimmuullaattee ccoonnttrraaccttiioonnss ooff ssmmooootthh mmuussccllee ooff aarrtteerriiaall vveesssseellss aanndd ccaauussee ccoonnssttrriiccttiioonn ooff tthheeiirr lluummeenn.. EExxaammpplleess:: nniiccoottiinnee,, aa nnuummbbeerr ooff mmeeddiicciinneess ((mmeezzaattoonnee,, eepphheeddrriinnee,, aaddrreennaalliinnee ddeerriivvaattiivveess,, aallccoohhooll ddeehhyyddrrooggeennaassee,, aannggiiootteennssiinn)).. 33)) BBiioollooggiiccaall ffaaccttoorrss:: bbiioollooggiiccaallllyy aaccttiivvee ssuubbssttaanncceess hhaavviinngg vvaassooccoonnssttrriiccttiivvee eeffffeeccttss ((ee..gg.. ccaatteecchhoollaammiinneess,, aannggiiootteennssiinn IIII,, aallccoohhooll ddeehhyyddrrooggeennaassee,, eennddootthheelliinn)),, bbiioollooggiiccaallllyy aaccttiivvee ssuubbssttaanncceess ooff mmiiccrroobbiicc oorriiggiinn,, tthheeiirr eexxoo-- aanndd eennddoottooxxiinnss,, mmeettaabboolliitteess hhaavviinngg aa vvaassooccoonnssttrriiccttiivvee eeffffeecctt..  AAccccoorrddiinngg ttoo iittss oorriiggiinn:: 11)) eennddooggeennoouuss 22)) eexxooggeennoouuss ((iinnffeeccttiioouuss aanndd nnoonniinnffeeccttiioouuss))..
    40. 40. PPaatthhooggeenneessiiss TThheerree aarree tthhrreeee mmeecchhaanniissmmss ooff ddeevveellooppmmeenntt iisscchheemmiiaa::  ccoommpprreessssiivvee –– ccoommpprreessssiioonn ooff aarrtteerriiaall vveesssseellss bbyy ttuummoorrss,, ssccaarrss,, lliiggaattuurreess,, eettcc..  oobbttuurraattiivvee –– oocccclluussiioonn ooff lluummeenn vveesssseellss bbyy tthhrroommbbuuss,, eemmbboolluuss,, eettcc..  aannggiioossppaassttiicc –– ssppaassmm ooff vveesssseellss aafftteerr eexxcciittaattiioonn αα-- aaddrreennoorreecceeppttoorrss oorr HH11-- rreecceeppttoorrss,, uunnddeerr tthhee iinnfflluueenncceess ooff vvaassoopprreessssiinn ((aannttiiddiiuurreettiicc hhoorrmmoonnee)),, TTxxAA22,, eennddootteelliinn‑‑11,, aannggiiootteennssiinn IIII,, PPgg HH22,, FF22αα,, GG22,, LLtt BB44,, CC44,, DD44,, EE44..
    41. 41. TThheerree aarree tthhrreeee ssttaaggeess iinn ppaatthhooggeenneessiiss ooff iisscchheemmiiaa..  11)) ddiissooddeerrss ooff eenneerrggeettiicc mmeettaabboolliissmm,, aass rreessuulltt ooff aaccttiivvaattiioonn ooff aannaaeerroobbiicc ooxxiiddaattiioonn wwiitthh pprroodduuccee llaaccttiicc aanndd ppyyrruuvviicc aacciiddss,, ddiissoorrddeerrss ooff KKrreebb''ss ccyyccllee aanndd pphhoosspphhoorryyllaattiivvee pprroocceesssseess wwiitthh iinnssuuffffiicciieennccyy ooff AATTPP,, ddeevveellooppmmeenntt ooff aacciiddoossiiss..  22)) ddiissoorrddeerrss eenneerrggeettiicc ddeeppeennddiinngg pprroocceesssseess oonn tthhee cceellll.. TThhaatt ddiissppllaayyss bbyy ddiissoorrddeerrss ssppeecciiffiicc ffuunnccttiioonn ooff cceellll ((ttrraaccttiioonn,, ttrraannssppoorrtt,, sseeccrreettoorryy)),, ddiissoorrddeerrss ooff eelleeccttrroollyyttiicc ppuummppss,, aaccttiivvaattiioonn ooff mmeemmbbrraanneess pphhoosspphhoolliippaasseess →→ ddeessttrruuccttiioonn ooff mmeemmbbrraannee aanndd cceellll oorrggaanneellss,, ddeeccrreeaassee pprroodduuccttiioonn ooff aallbbuummiinnss.. AAllll tthhiiss pprroocceesssseess ffiinniisshheedd bbyy nneeccrroobbiioottiicc cchhaannggeess aanndd ffoorrmmeedd rreeggiioonnss ooff nneeccrroossiiss..  33)) aaccttiivvaattiioonn pprroodduuccttiioonn ssoommee eelleemmeennttss ooff ccoonnnneeccttiivvee ttiissssuuee:: ccoollllaaggeenn,, ggllyyccoopprrootteeiinnss,, eettcc.. TThhaann aaccttiivvaattee sscclleerroottiicc pprroocceesssseess ooff nneeccrroossiiss hhoottbbeedd..
    42. 42. CClluubbbbiinngg is caused by decreased oxygenation, which leads to fibrous tissue hyperplasia in the area between the nail and distal portion of each digit, associated with lymphocytic extravasation, increased vascularity, and edema.
    43. 43. SSttaassiiss –– decrease or stop blood flow in capillaries, small arteries and venues Distinguish some types of stasis: • ischemic • venous aarree ccaauusseedd bbyy aaccccoorrddiinnggllyy iisscchheemmiiaa aanndd • vveennoouuss hhyyppeerreemmiiaa capillary (primary) • RReeaassoonnss ooff ccaappiillllaarryy ssttaassiiss: 1) physical (high – more than 80ºC, and low less than -7ºC temperature), 2) chemical (poisons, turpentine, mustard oil), 3) biological (toxins of microorganisms). • PPaatthhooggeenneessiiss.. Capillary stasis is caused by aggregation of blood cells, edema of endothelium cells, blood flow decreased, clotting of blood as result of increase of permeability of vascular walls (under the action of histamine, serotonin, heparin) • The final stage of stasis involves the process of aggregation and agglutination of the corpuscular elements of blood which results in blood thickening and its fluidity reduction. This process is activated by proaggregants, cations and high molecular weight proteins.
    44. 44. MMaanniiffeessttaattiioonnss ooff ssttaassiiss • reduction of the inner diameter in ischemic stasis; • increase of the lumen of vessels of microcirculation in congestive stasis; • increased number of aggregates of blood corpuscles in the lumen of vessels and on their walls; • microhemorrhages (more often in congestive stasis). The consequences of stasis. * When agents causing stasis are quickly withdrawn blood flow in the vessels of microcirculation is restored without entailing any noticeable changes in tissues. * Prolonged stasis results in dystrophyc changes in tissues (quite often to death of a tissue site or an organ).
    45. 45. Embolus and embolism • Embolism – is a pathological processes, which characterized by traveling of free bodies (embolus) in the vessels. An embolus is a substance that circulates from one location in the body to another, through the bloodstream. • By origin emboles: 1) exogenous (air, gas, foreign bodies, bacteria etc) 2) endogenous (thrombus, amniotic fluids, fat, tumor cells etc.) • There are tthhrreeee mmaaiinn ttyyppeess ooff eemmbboolliissmm:: 1) embolism of lesser [ppuullmmoonnaarryy] circulation, 2) embolism of greater [ssyysstteemmiicc] circulation, 3) embolism of ppoorrttaall vveeiinn.
    46. 46. Embolism ooff ppuullmmoonnaarryy cciirrccuullaattiioonn • Embols that originate in the venous circulation, such as from deep vein thrombosis, travel to the right side of the heart to the pulmonary circulation and eventually causing pulmonary infarction and even death. • This syndrome characterized by: 1) generalized spasm of vessels pulmonary circulation → acute hypertension into pulmonary circulation and develop acute insufficiency of right heart; 2) abrupt decrease of blood pressure in systemic circulation, as result of decreasing cardiac output and general peripheral resistance; 3) disorders of external respiration → develop of respiratory failure.
    47. 47. Embolism of ssyysstteemmiicc cciirrccuullaattiioonn • Reasons: often is a thrombus, what is formed in the left side of heart (as result of coarctation of aorta, aortic aneurysm, fibrillation, operation on the heart and artificial valves), air or fat emboli. • Consequences depend on thrombus location. • Coronary artery → infarction of heart; • renal artery → infarction of kidney; • arteries of lower extremities → gangrene, etc.
    48. 48. EEmmbboolliissmm ooff ppoorrttaall vveeiinn Characterized by development of portal hypertension, that displays by ttrriiaadd ssiiggnn: 11)) aasscciitteess, (abdominal [peritoneal] dropsy), 22)) ccaappuuttee mmeedduussaaee – varicose veins of front wall of abdomen, veins of gullet (esophagus), and rectal veins, 33)) sspplleennoommeeggaallyy.
    49. 49. • TTuummoorr eemmbboolliissmm is the way in which malignant tumors spread from the site of origin to distant metastatic sites using the bloodstream. • The malignant tumor infiltrates through the wall of blood vessels (usually a venule or vein) at the primary site to occupy the lumen, and clumps of tumor cells break off and are carried in the venous system until they reach a vessel too small to permit further passage, than impact there and often grow to produce a distant metastasis. • FFaatt aanndd bboonnee mmaarrrrooww eemmbboolliissmm may occur following severe fracture trauma of bones, fragments of fat released from traumatized adipocytes is the fatty bone marrow may enter the blood circulation through thin-walled veins torn by the fracture trauma. • They pass trough the venous system to the right side of the heart, and then via pulmonary arteries to the lung capillaries, where some are trapped. EEmmbboolliissmm Tumor embolus in the main pulmonary artery
    50. 50. EEmmbboolliissmm • AAiirr eemmbboolliissmm iiss uussuuaallllyy dduuee ttoo aacccciiddeennttaall ppuummppiinngg ooff aaiirr iinnttoo tthhee vveennoouuss cciirrccuullaattiioonn dduurriinngg iinnttrraavveennoouuss iinnjjeeccttiioonn oorr ttrraannssffuussiioonn.. IIff llaarrggee qquuaannttiittiieess ooff aaiirr mmiixxeedd wwiitthh bblloooodd eenntteerr tthhee rriigghhtt aattrriiuumm,, aa bbllooooddyy ffrrootthh iiss ffoorrmmeedd aanndd tthhee ppaattiieenntt mmaayy ssuuffffeerr ccaarrddiiaacc aarrrreesstt.. • IInn ddeeeepp--sseeaa ddiivveerrss,, iinnhhaalleedd aaiirr mmaayy ddiissssoollvvee iinnttoo tthhee ppllaassmmaa dduuee ttoo tthhee iinnccrreeaasseedd pprreessssuurree aatt ggrreeaatt ddeepptthhss,, oonnllyy ttoo rreeffoorrmm iinnttoo bbuubblleess ooff ggaass (ggaass eemmbboolliissmm) wwiitthhiinn tthhee cciirrccuullaattiioonn iiff tthhee ddiivveerr ccoommeess ttoo tthhee ssuurrffaaccee ttoooo qquuiicckkllyy.. TThhiiss ddeeccoommpprreessssiioonn ssiicckknneessss aanndd eemmbboolliizzaattiioonn ooff tthhee bbuubbbblleess ooff mmaaiinnllyy nniittrrooggeenn ggaass mmaayy oocccclluuddee ssmmaallll vveesssseellss,, lleeaaddiinngg ttoo wwiiddeesspprreeaadd aannooxxiiaa ooff ttiissssuueess,, aanndd eevveenn ddeeaatthh.. • AAmmnniioottiicc fflluuiidd eemmbboolliissmm mmaayy ooccccuurr rraarreellyy dduurriinngg cchhiillddbbiirrtthh;; ssoommee ooff tthhee aammnnooiioottiicc fflluuiidd ((ccoonnttaaiinniinngg ffeettaall cceellllss ffrroomm tthhee sskkiinn ssuurrffaaccee)) mmaayy eenntteerr tthhee mmaatteerrnnaall cciirrccuullaattiioonn tthhrroouugghh tthhee eexxppoosseedd aanndd bblleeeeddiinngg ppllaacceennttaall bbeedd iinn tthhee uutteerruuss.. TThhee mmaatteerriiaall ppaasssseess iinn tthhee vveennoouuss cciirrccuullaattiioonn ttoo tthhee lluunngg ccaappiillllaarriieess aanndd mmaayy ccaauussee aaccuuttee aallvveeoollaarr wwaallll ddaammaaggee aanndd disseminated intravascular coagulation.
    51. 51. RReettrrooggrraaddee eemmbboolliissmm:: embolism of a vein by an embolus carried in a ddiirreeccttiioonn ooppppoossiittee to that of the normal blood current, after being diverted into a smaller vein. SYN: venous embolism.
    52. 52. • TThhrroommbboossiiss – is a life-time processes to produce of thrombus in the vessel's lumen. A thrombus is a blood clot, consisting of platelets, fibrin, and a red and white blood cells, that forms anywhere within the vascular system, such as the arteries, veins, heart chambers or heart valves. TThhrreeee ccoonnddiittiioonnss,, kknnoowwnn aass VViirrcchhooww'ss ttrriiaadd,, pprroommoottee tthhrroommbbuuss ffoorrmmaattiioonn:: 1) Endothelial injury, 2) Alterations in laminar blood flow (slugging blood flow : hanges in laminar flow, turbulence → arterial thrombosis, changes to stasis of flow → venous thrombosis) 3) Increased coagulability or decreased activity of anticoagulative and fibrinolytic systems.
    53. 53. TTyyppeess ooff tthhrroommbbuuss • PPaarriieettaall [[mmuurraall tthhrroommbboossiiss]] aanndd oobbssttrruuccttiivvee. • WWhhiittee,, rreedd aanndd mmiixxeedd [[ccoommpplleexx]] TThheerree aarree ttwwoo pphhaasseess ooff bblloooodd cclloottttiinngg:: 1) cellular, 2) plasmatic. aaddhheessiioonn,, • Cellular phase consist of aaggggrreeggaattiioonn,, of platelets. aagggglluuttiinnaattiioonn • Plasmatic phase consist of several successive [consecutive, cascade] reactions, results of which is creation of ffiibbrriinn
    54. 54. TThhrroommbbuuss BBlloooodd CClloott ((PPoossttmmoorrtteenn)) CCoonnssiisstteennccyy DDrryy aanndd FFrriiaabbllee MMooiisstt aanndd JJeellllyy--lliikkee SSuurrffaaccee GGrraannuullaarr aanndd RRoouugghh SSmmooootthh aanndd gglliisstteenniinngg CCoolloorr WWhhiittee aanndd BBuuffff IInntteennssee rreedd oorr yyeellllooww LLooccaattiioonn IInnttrraavvaassccuullaarr EExxttrraavvaassccuullaarr oorr iinnttrraavvaassccuullaarr ((ppoossttmmoorrtteenn)) EEnnddootthheelliiuumm DDaammaaggeedd//iinnjjuurreedd UUnnddaammaaggeedd CCoommppoossiittiioonn PPllaatteelleettss ((pprriimmaarriillyy)) FFiibbrriinn RRBBCCss aanndd WWBBCCss LLaacckkss ppllaatteelleettss FFiibbrriinn ((pprriimmaarriillyy)) RRBBCCss aanndd WWBBCCss RRaappiiddiittyy ooff bblloooodd ffllooww FFoorrmmeedd iinn fflloowwiinngg ssttrreeaamm ooff bblloooodd FFoorrmmeedd iinn ssttaaggnnaanntt ccoolluummnn ooff bblloooodd LLiinneess ooff ZZaahhnn PPrreesseenntt AAbbsseenntt SShhaappee HHaass sshhaappee LLaacckkss sshhaappee AAttttaacchheedd ttoo tthhee vveesssseell wwaallll yyeess nnoo OOrrggaanniizzaattiioonn MMaayy bbee ppaarrttiiaallllyy oorrggaanniizzeedd NNoo oorrggaanniizzaattiioonn
    55. 55. CCoonnsseeqquueenncceess ooff tthhrroommbboossiiss - iisscchheemmiiaa,, - nneeccrroossiiss,, - ttrroopphhiicc ddiissoorrddeerrss,, - rreeccaannaalliizzaattiioonn,, - sseeppttiicc mmeellttiinngg [[ddiissssoolluuttiioonn]],, - ccaallcciiffiiccaattiioonn eettcc..
    56. 56. Literature • Robbins and Cotran Pathologic Basis of Disease 9th edition./ Kumar, Abbas, Fauto. – 2013. – Chapter 2. • General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simferopol. – 2011. • Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Ch. 9. • Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. • Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– New York, Milwaukee. – 2009. • Pathophysiology, N.K. Symeonova. Kyiv, AUS medicine Publishing. – 2010.
    57. 57. Manage your Time..!

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