Blood and Lymph Circulation Disorders – Hyperemia, Bleeding, Thrombosis

DISORDERS OF BLOOD AND LYMPH CIRCULATION – In a healthy organism, normal blood and lymph circulation is closely related to each other and is determined by the activity of the heart as a source of blood flow, vessels – a source of blood distribution and lymph collection; microcirculatory bed – a springboard for transcapillary metabolism and tissue metabolism.

The function of the circulatory and lymphatic systems is provided by the mechanisms of neurohumoral regulation, which are aimed at maintaining homeostasis – the relative dynamic constancy of the internal environment.

Disorders of blood and lymph circulation and their neurohumoral regulation lead to disruption of tissue metabolism, which leads to damage to tissue structure (alteration), the development of either type of dystrophy or necrosis.

In case of damage at the level of the heart, there are general, at the level of blood vessels – local disorders of blood and lymph circulation. Local circulatory disorders (eg myocardial infarction) can cause general disorders.

DISORDERS OF BLOOD CIRCULATION OR Disorders of blood and lymph circulation

Circulatory disorders can be divided into 3 groups:
1) violations of blood circulation: plethora (arterial or venous) and anemia;
2) violations of the permeability of the vascular wall: bleeding (hemorrhage) and plasmorrhage;
3) disorders of blood flow and rheological state of blood: stasis, sludge phenomenon, thrombosis, and embolism.

In the fetus, newborn, and child of the first 3 years of life, general and local plethora, anemia, hemorrhages, stasis occurs faster and more often than in adults, which depends on the immaturity of the regulatory mechanisms of blood circulation. Thrombosis and heart attack are less common in children than in adults. These circulatory disorders occur mainly in connection with malformations of the cardiovascular system, the addition of a secondary septic infection to them, or in some acute infectious diseases (diphtheria, viral myocarditis, etc.).

PLETHORA OR HYPEREMIA

Congestion (hyperemia), depending on the spread of the process, can be arterial and venous.

Arterial plethora

Arterial plethora – increased blood filling of an organ, tissue due to increased arterial blood flow. It can be physiological and pathological, general and local.
Physiological arises under the action of adequate doses of physical and chemical factors, feelings of anger, bashfulness (reflex hyperemia), with increased organ function (working hyperemia), when climbing to a height (climbers).

An example of pathological general arterial hyperemia is erythremia – a type of chronic leukemia for which a characteristic real plethora (from Greek – “overflow”) is an increase in the total mass of blood mainly due to erythrocytes. In such cases, there is a red color of the skin and mucous membranes, an increase in blood pressure. There is also a hydraemic plethora (total blood mass, mainly due to plasma and kidney problems).

More often, arterial hyperemia is of local nature and arises from a variety of reasons.

Depending on the etiology and developmental mechanisms, the following types of pathological local arterial hyperemia are distinguished:
1) angioneurotic (neuroparalytic);
2) collateral;
3) hyperemia after anemia (post-anemic);
4) vacant;
5) inflammatory;
6) hyperemia against the background of an arteriovenous shunt.

Angioneurotic (neuroparalytic) hyperemia occurs due to irritation of the vasodilating nerves or paralysis of the vasoconstrictor nerves. The skin, mucous membranes become red, slightly swollen, when touched – warm or even hot. Occurs in some parts of the body with a violation of innervation; on the skin and mucous membranes of the face with infectious diseases (flu, eruptions), in which the nodes of the sympathetic nervous system may be damaged; neuralgia – this type of hyperemia passes quickly, without consequences.

Collateral hyperemia occurs due to the obstruction of blood flow through the main arterial trunk, closed by a thrombus, embolus, ligature. In such cases, the blood is directed through the collateral vessels. Their lumen reflexively expands, the flow of arterial blood increases and the tissue receives an increased amount of blood.

Hyperemia after anemia (post-anemic) develops when the factor that caused the clamping of the artery (tumor, fluid accumulation in cavities, ligature, etc.) and tissue anemia is quickly eliminated. In such cases, the vessels of the previously exsanguinated tissue sharply expand and overflow with blood, which can lead not only to their rupture and hemorrhages but also to anemia of other organs, for example, the main brain, due to a sharp redistribution of blood. Therefore, such manipulations as removing fluid from body cavities, large tumors, removing an elastic tourniquet should be carried out slowly.
Vacant hyperemia (from Lat. Vacuus – empty) develops due to a decrease in barometric pressure. It can be common, for example, among divers during a rapid ascent from a place of high pressure. The hyperemia that occurs, in this case, is combined with gas embolism, vascular thrombosis, and hemorrhages.
Local vacuum hyperemia appears on the skin under the influence of medical cups, which form a rarefied space (vacuum) over certain areas.
Inflammatory hyperemia is a constant companion of inflammation, it is based on inadequate production of biologically active substances.
Hyperemia due to arteriovenous shunt occurs with a gunshot injury or other injury, as a result of which a message is formed between the artery and the vein, then arterial blood is directed to the vein.
The value of pathological arterial hyperemia is determined by its type. Collateral hyperemia is inherently compensatory and provides blood circulation when the arterial trunk is closed; this must be taken into account in surgical practice: so dressing a. femoralis below branch a. profundal femoris (deep ar. thigh) is compensated, and if bandaged higher – gangrene of the limb may occurInflammatory hyperemia is an indispensable component of a protective and adaptive reaction. With pathologically altered vessels (especially in elderly people), hyperemia can cause wall rupture. Vacant hyperemia is one of the components of decompression sickness.

Venous congestion

Venous congestion – increased blood filling of an organ or tissue due to a violation (decrease) of blood outflow; blood flow is not changed or reduced. Venous congestion can be general and local.

General venous congestion

General venous congestion develops in diseases of the cardiovascular system, can be acute and chronic.

In acute general venous plethora, which is a manifestation of the syndrome of acute heart failure (insufficiency of myocardial contractility, for example, with myocardial infarction, acute myocarditis), due to hypoxic damage to histohematogenous barriers and a sharp increase in capillary permeability in tissues, plasma impregnation (plasmorrhage) is observed, stasis in the capillaries and multiple diapedetic hemorrhages; dystrophic and necrotic changes develop in the parenchymal organs.

  • In acute venous congestion, edema and hemorrhages occur in the lungs – one of the main causes of death in patients with acute cardiovascular failure.
  • In the kidneys – dystrophic and necrotic changes, especially the epithelium of the tubules.
  • In the liver – centrilobular hemorrhages and necrosis.

Chronic general venous congestion is often a manifestation of the syndrome of chronic cardiovascular insufficiency, which complicates many chronic heart diseases (heart defects, coronary heart disease, chronic myocarditis, myocardiopathies, endocardial fibroelastosis, pneumosclerosis of various origins, etc.).
Organ changes in chronic venous stasis: The skin, especially the lower extremities, becomes cold and bluish in color (cyanosis). Veins of the skin and subcutaneous tissue are dilated, filled with blood; dilated and congested lymph and lymphatic vessels. Edema of the dermis and subcutaneous tissue, the development of connective tissue in the skin. In connection with venous congestion, edema, and sclerosis, inflammatory processes and ulcers occur in the skin, which does not heal for a long time.

  • LiverMacroscopically: in chronic venous stasis it is enlarged, dense, rounded edges, the cut surface is gray-yellow with dark red specks, similar to nutmeg, therefore such a liver is called “nutmeg”Microscopically: a plethora of the central sections of the lobules, where hepatocytes are destroyed, these areas on the cut of the liver are dark red. On the periphery of the lobules, liver cells are in a state of dystrophy, often fatty, which explains the gray-yellow color of the liver tissue.
    • Morphogenesis of liver changes with prolonged venous stasis: Due to the decompensation of cardiac activity, the right ventricle is not able to pump blood in full into the pulmonary artery, therefore stagnation occurs in the inferior vena cava system, which passes to the hepatic veins and further spreads to the combined and central veins, and then to the sinusoids. This is what explains the selective plethora of the center of the lobules.
    • Sinusoids expand only in the central parts of the lobules, and in other parts, they meet resistance from the capillary branches of the hepatic artery flowing into the sinusoid, where the pressure is higher than in the sinusoids. As the plethora increases in the center of the lobules, hemorrhages appear; in hepatocytes, dystrophy, atrophy, and necrosis develop. Hepatocytes of the periphery of the lobules compensatory hypertrophy, some with the development of fatty degeneration.
    • In the area of ​​hemorrhages and dead hepatocytes, the proliferation of connective tissue occurs, which is associated with the proliferation of sinusoid cells – lipocytes, which can act as fibroblasts, and near the central and collecting veins – with the proliferation of adventitia fibroblasts of these veins. Due to the proliferation of connective tissue in the sinusoids, a continuous basement membrane appears (it is absent in the normal liver), that is, capillarization of the sinusoids occurs, a capillary-parenchymal block occurs, which increases hypoxia, leads to the progression of atrophic and sclerotic changes in the liver, against the background of venous stasis, lymphostasis develops – this is how congestive fibrosis (sclerosis) of the liver is formed.
    • With the progressive development of connective tissue, incomplete regeneration of hepatocytes appears with the formation of regenerate nodes, restructuring, and deformation of the organ. Stagnant (nutmeg) cirrhosis of the liver develops, which is also called cardiac, since it occurs in chronic heart failure. Cirrhosis is an overgrowth of connective tissue with subsequent deformation of the organ.
  • In the lungs with chronic venous plethora, two types of changes occur – multiple hemorrhages, which cause hemosiderosis of the lungs, and the development of connective tissue, that is, sclerosis. The lungs become large, brown, and dense – brown induration of the lungs.
  • There is an idiopathic brown induration of the lungs (idiopathic, or essential hemosiderosis of the lungs, Celen-Gelerstedt syndrome). This disease is rare, mainly in children aged 3 to 8 years. The morphogenesis of essential hemosiderosis of the lungs does not fundamentally differ from the brown compaction of the lungs. However, hemosiderosis is much more pronounced and is often accompanied by multiple hemorrhages. The cause of the disease is considered to be the primary underdevelopment of the elastic frame of the pulmonary vessels, as a result of which vascular aneurysms, blood stasis, and diapedetic hemorrhages occur in the lungs; the role of infectious diseases, intoxications, allergies, and auto immunization is not excluded.
  • Kidneys in chronic venous stasis – enlarged, dense and cyanotic – cyanotic induration of the kidneys; in particular, the veins of the medulla and the border zone are full-blooded. Against the background of venous stasis, lymphostasis develops. In conditions of increasing hypoxia, dystrophy of the nephrocytes of the main divisions of the nephron and sclerosis occur.
  • Chronic venous congestion in the spleen also leads to its cyanotic induration. It is enlarged, dense, dark cherry color; follicular atrophy and pulp sclerosis are determined. With general chronic venous stasis, cyanotic induration is inherent in other organs as well.

Consequences and significance. General venous congestion is a reversible process if its cause is promptly eliminated. It has a negative meaning for the body since the function of organs decreases under conditions of prolonged hypoxia. A prolonged state of tissue hypoxia in chronic general venous congestion leads to irreversible degenerative, atrophic, and sclerotic processes.

 

Local venous plethora (hyperemia)

Local venous plethora (hyperemia) is observed when the outflow of venous blood from one or another organ or part of the body is obstructed.

Based on the etiology and development mechanism, they are distinguished:

  1. Obstructive venous hyperemia due to the closure of the lumen of the vein (thrombus or embolus): obliterating thrombophlebitis of the hepatic veins, which is characteristic of the disease (syndrome) Bada-Chiari, in which, as with general venous congestion, muscat liver and muscat cirrhosis can developcyanotic induration of the kidneys with renal vein thrombosis; venous congestion and edema of the extremity with vein thrombosis, with portal vein thrombosis – venous congestion of the intestine and all unpaired organs.
  2. Compression – when the vein is compressed from the outside (tumor, edema, ligature, developed connective tissue).
  3. Collateral – as a result of the development of venous collaterals with difficulty or cessation of blood outflow along the main venous highways (for example, portocaval anastomoses in case of impaired blood outflow through the portal vein). Collateral veins overflowing with blood expand sharply, and their wall becomes thin, which can provoke hemorrhages (for example, from dilated and thinned veins of the esophagus, hemorrhoids in liver cirrhosis).

Consequences: plasmorrhagic, dystrophic, atrophic, and sclerotic changes, the development of venous (congestive) heart attacks.

 

Anemia (Blood Disorder)

Anemia, or ischemia (from the Greek. Isho – to delay) is a decrease in the blood volume of a tissue, organ, part of the body due to a reduced blood flow. ‘

 

General anemia

General anemia – anemia. Will be studied further. Tissue changes that occur with anemia are associated with hypoxia or anoxia, that is, oxygen starvation.

 

Local anemia

Local anemia can be acute or chronic. The consequences of acute anemia are dystrophy and necrosis. Ischemic necrosis is called “infarction”. For the microscopic diagnosis of ischemia, various tetrazolium salts, potassium telurite are used, which, outside the ischemic areas (where the activity of dehydrogenases is high), are restored and stain the tissue gray or black, while the ischemic areas (where the enzyme activity is reduced or absent) remain unstained. Based on the data of an electro-histochemical study of tissue changes in acute anemia and in heart attack, acute ischemia should be considered as a prenecrotic (pre-infarction) state.
In chronic anemia, atrophy and sclerosis develop due to an increase in the collagen-synthesizing activity of fibroblasts.

Depending on the causes and conditions of occurrence, anemia is divided into the following types:

  1. angiospastic;
  2. obstructive;
  3. compression;
  4. due to blood redistribution.
  • Angiospastic anemia occurs due to artery spasm due to the influence of various stimuli. The main mechanisms of angiospasm are extracellular under the influence of vasoconstrictors (catecholamines, serotonin) and intracellular, associated with a violation of the redistribution of calcium ions. It occurs with the action of a painful stimulus, vasoconstrictor drugs (adrenaline), with negative emotional effects.
  • Obstructive anemia develops as a result of thrombosis or embolism, with the proliferation of connective tissue in the lumen of the artery with inflammation of its wall (obliterating endarteritis), narrowing of the lumen of the artery by an atherosclerotic plaque.
  • Compression anemia appears when an artery is compressed by a tumor, tourniquet, ligature, etc.).
  • Ischemia due to redistribution of blood is observed in cases of hyperemia after anemia (see Arterial plethora). Such is, for example, ischemia of the main brain when fluid is released from the abdominal cavity, where a significant amount of blood flows.

 

Bleeding (hemorrhage) – (Blood Disorder)

Bleeding (hemorrhage) is the release of blood from the lumen of a blood vessel or heart cavity into the environment ( external bleeding) or into the body cavity ( internal bleeding). Examples of external bleeding can be hemoptysis (haemoptoa), nosebleeds (epistaxis), vomiting of blood (haemothenesis), blood in the stool (melaena), bleeding from the uterus (metrorrhagia). With internal bleeding, blood can accumulate in the pericardial cavity (hemopericardium), pleura (hemothorax), and abdominal cavity (hemoperitoneum). If during bleeding, blood accumulates in the tissues, then they talk about hemorrhages. The accumulation of coagulated blood in tissue with a violation of its integrity is called a hematoma, and if tissue elements are preserved, it is called hemorrhagic impregnation (hemorrhagic infiltration).

Flat hemorrhages, for example, in the skin, mucous membranes, are called bruises, and small drip hemorrhages are called petechiae, or ecchymosis.
Depending on the source: arterial, venous, capillary, parenchymal.

Causes and mechanisms of bleeding:

  1. Rupture of the wall of the heart or vessel (hemorrhagic reg hekhin from Lat. Geho – rupture): in case of injury, trauma to the wall or the development in it of such pathological processes as necrosis (infarction), inflammation, or sclerosis: the rupture of the heart during myocardial infarction, wall ruptured aortic aneurysms in syphilis, atherosclerosis. Bleeding during vascular injury is divided into primary and secondary. Primary bleeding occurs at the moment of injury, secondary – after some time due to suppuration of the wound and melting of a blood clot, which closed the vessel defect.
  2. Corrosion of the vessel wall (hemorrhagic reg diabrosin, from the Greek diabrosis – arosia, corrosion) – erosive bleeding occurs: with caseous necrosis in the wall of the cavity with tuberculosis, gangrenous appendicitis, gastric ulcer, ulceration of a cancerous tumor (with an extravaginal tube) when the chorionic villi germinate and erode the wall of the fallopian tube and its vessel.
  3. Increase in the permeability of the vessel wall (hemorrhagic reg diapedesis, from the Greek dia – through, redao – jumping): with angioedema, changes in microcirculation, tissue hypoxia. With brain damage, arterial hypertension, systemic vasculitis, infectious and infectious-allergic diseases, diseases of the blood system (hemoblastosis and anemia), coagulopathies. When diapedetic hemorrhages become systemic, they become a manifestation of the hemorrhagic syndrome.

Consequences of bleeding (hemorrhage): resorption of blood, the formation of cysts at the site of hemorrhage (eg, in the brain), encapsulation or invasion of hematoma by connective tissue, accession of infection, and suppuration.

The value of bleeding is determined by its type and cause, the amount of lost blood, the rate of blood loss. When blood loss is within 500-700 ml, about 10% of the BCC is compensated. The development of hemorrhagic shock is caused by hemorrhages, in which blood loss exceeds 1000 ml (1 liter), more than 20% of the BCC. Blood loss that exceeds 50% of the BCC is fatal.

Bleeding for several days can also lead to significant blood loss and death (death from acute anemia). Long-term bleeding that recurs periodically (for example, with gastric ulcer and 12-p. Intestine, hemorrhoids) can cause chronic anemia (posthemorrhagic anemia). The importance of hemorrhage for the body largely depends on the location. Particularly dangerous, often fatal, there is a hemorrhage in the brain (a manifestation of hemorrhagic stroke in hypertension, rupture of an aneurysm of the cerebral artery, aorta, heart wall, arosia of the vessel in the wall of the tuberculous cavity).

Plasmorrhage (Blood Disorder)

Plasmorrhage is the exit of plasma beyond the boundaries of the bloodstream.

Microscopically, upon plasma impregnation, the arteriole wall becomes thickened and homogeneous.

Development mechanism:

  1. damage to the vessels of the microvasculature due to spasm, tissue hypoxia, immunopathological reactions
  2. changes in blood constants: an increase in the plasma content of vasoactive substances (histamine, serotonin), natural anticoagulants (heparin, fibrinolysin), coarse proteins, lipoproteins, impaired rheological properties.

Plasmorrhage is often found in hypertension, atherosclerosis, decompensated heart disease, infectious, infectious-allergic, and autoimmune diseases. The consequence of plasmorrhagia is the impregnation of the vessel wall and the tissues that surround it with blood plasma – plasma impregnation. The consequence of plasma impregnation is fibrinoid necrosis and vascular hyalinosis. The value of plasmorrhage consists in a violation of transcapillary metabolism with subsequent changes in the structure of organs and tissues.

Stasis

Stasis – (from Latin – stop) – stopping blood flow in the vessels of the microvasculature, mainly in the capillaries. The arrest of blood flow begins slowly, which is defined as prestasis.

Microscopically: the lumen of the vessels is dilated, filled with deformed erythrocytes in the form of coins, the endothelium with edema, little plasma. Blood clotting during stasis does not occur. With the complete overlap of the lumen of the vessel, stasis is difficult to distinguish from the sludge phenomenon. Sludge phenomenon (from the English sludge – mud) – the adhesion of erythrocytes to aggregates. Microscopically, the main sign of the sludge phenomenon is that in the lumen of the vessel between the dense aggregate of erythrocytes and the wall, there remains a lumen filled with plasma and blood elements.

Development mechanism. The development of stasis is based on dis-circulatory changes that occur when:

  1. violation of the rheological properties of blood as a manifestation of enhanced intra-capillary aggregation of erythrocytes.
  2. violation of the physical and chemical properties of erythrocytes;
  3. a change in the composition of blood proteins due to an increase in coarse fractions
  4. venous congestion (congestive stasis)
  5. ischemia (ischemic stasis),
  6. violation of the innervation of the microvasculature
  7. inflammatory changes in the capillaries.

Reasons: circulatory disorders due to the influence of physical (high temperature, cold) and chemical (acid, alkali) factors; with infectious (malaria, typhus), infectious-allergic and autoimmune (rheumatic diseases) diseases, diseases of the heart and blood vessels (heart defects, coronary heart disease).

The value of stasis depends not only on the duration but also on the sensitivity of the organ or tissue to oxygen starvation (brain). Stasis is a reversible phenomenon; the state of the vessels after the termination of stasis is called post stasis; irreversible stasis results in necrobiosis and tissue necrosis.

DIC syndrome (Blood Disorder)

Disseminated intravascular coagulation syndrome (disseminated intravascular coagulation syndrome, thrombo-hemorrhagic syndrome, consumption coagulopathy) is a universal nonspecific reaction that develops in several severe pathological conditions. It is based on the discoordination of the functions of the coagulation and anti-coagulation blood systems, which are responsible for hemostasis.

DIC often occurs as a complication of many diseases and accompanies all types of shock.

  1. Obstetric pathology: with massive uterine bleeding, rupture, and detachment of the placenta, cesarean section, cystic drift.
  2. Significant trauma and tissue damage, operations on organs that contain a large amount of thromboplastin (uterus, lungs).
  3. With leukemia and anemia, repeated massive blood transfusions.
  4. Infectious and autoimmune diseases (especially with sepsis), intoxication, shock, and others.

 

There are three special systems to maintain the liquid state of blood in the human body:

  1. Coagulant participates in the formation of a blood clot.
  2. Anticoagulant (anticoagulant), prevents the formation of a blood clot. These are antithrombin III (synthesized in the liver) and heparin (synthesized by mast cells).
  3. Fibrinolytic, dissolves the formed thrombus. This is fibrinolysin (plasmin), which is contained in the blood plasma in the form of a proenzyme – plasminogen)

 

Mechanism: At the heart of the DIC syndrome is the discoordination of the functions of the coagulation and anti-coagulation blood systems, which are responsible for hemostasis. In DIC syndrome, due to the release of a large amount of tissue or blood thromboplastin into the blood, the plasma and platelet links of hemostasis, the fibrinolytic and calicrein kinin systems are activated, after which their depletion occurs, which leads in severe cases to complete non-coagulation of blood.

Launcher – The mechanism in the development of DIC is the release of a large amount of tissue, or blood thromboplastin, into the blood. In this case, hypercoagulability and thrombogenesis occur. Massive thrombogenesis leads to irreversible platelet aggregation and intensive use of blood coagulation factors. Plasmin appears next to thrombin in the blood. Their presence in the blood with DVS-syndrome determines the formation of both fibrin monomer and the cleavage of fibrin to early and late degradation products. Some of them enter into a complex with the fibrin monomer, forming complexes of soluble fibrin, which loses its ability to polymerize. At the same time, some of the fibrin monomers polymerize, causing obstruction of blood flow in microvessels and causing tissue hypoxia. Fibrin deposited in microvessels captures platelets, thrombocytopenia develops, fibrin-erythrocyte reaction – hemolytic anemia. Under these conditions, the natural defense mechanisms of the anticoagulant system are depleted. Dysfunction of anticoagulant mechanisms, a high level of soluble fibrin complexes leads to hypercoagulation and hemorrhages.

Stages:

  1. Hypercoagulation.
  2. Hypocoagulation without fibrinolysis activation.
  3. Hypocoagulation with activation of fibrinolysis.
  4. Complete non-clotting of blood. If in the third stage the patient remains alive, then the recovery stage begins – the normalization of the state of the blood coagulation system.

Diagnostics: coagulogram indices, determination of PDP (fibrinogen degradation products) by ethanol test, platelet count. For phase I: blood clotting time decreases, positive ethanol test. For phase II: a decrease in the number of platelets to 120 by 10 9 / l. PDP and damaged erythrocytes are determined. In the III phase: the blood coagulation time is lengthened, the number of platelets decreases even more to 100 per 10 9 / l, rapid clot lysis. IV phase: a clot does not form, the number of platelets is less than 60 per 10 9 / l.

Morphologically: characterized by the formation of disseminated (scattered) blood clots (fibrin and erythrocytic, hyaline) in the microvasculature in combination with blood clotting, which leads to multiple massive hemorrhages.
Blood clots that form in the microvessels of the lungs, kidneys, pituitary gland, liver, brain, skin, adrenal glands, gastrointestinal tract, leading to necrosis and infarctions (cortical necrosis of the kidneys, heart attacks in the lungs, brain, pituitary gland, necrosis and hemorrhage in the adrenal glands, etc.) and are combined with multiple hemorrhages in the gastrointestinal tract: hemorrhages in the mucous membrane, erosion, acute ulcers, hemorrhages in the skin at the injection sites. Many organs become “shock”, hepatic, renal, pulmonary, adrenal insufficiency develops.