Pathology of blood circulation. (Edema, hyperemia, ischemia, hemorrhage, thrombosis, embolism).

Transcription

1 Lecture # 4 General medicine Faculty Pathology of blood circulation. (Edema, hyperemia, ischemia, hemorrhage, thrombosis, embolism). Prepared by: Associate Professor, Ph.D. R. Deev Kazan, 2018 M.Mavlikeev. MD

2 The pathology of the circulation (hemodynamic disorders) includes: Edema Violations of the blood volume Violation of the permeability of the vascular wall Disturbance of blood flow Edema Anasarca Hydrotorax Hydropericardium Ascites (hydroperitoneum) Arterial hyperemia Venous plethora (acute / chronic) Anemia (Ischemia) (acute / chronic) Bleeding Hemorrhage Plasmorrhagia Stasis Thrombosis Embolism

3 1. Edema - accumulation of tissue fluid in serous cavities, or stroma of organs. Mechanisms of formation Hydrostatic pressure in capillaries Terminal arteriole Capillary In the thoracic duct and eventually into the left subclavian vein Increased interstitial fluid pressure Colloid-osmotic plasma pressure Postcapillary venule 1 - Increased hydrostatic pressure in capillaries; 2 - Low osmotic pressure of plasma; 3 - Sodium and water retention; 4 - Lymphatic obstruction; 5 - Increased permeability of the vascular wall. Classification Depending on the pathological condition, which is accompanied by edema, edema may be: traumatic allergic inflammatory toxic congestive lymphatic oncotic (including cahetical) dysmetabolic

4 Edema

5 General edema Hydrostatic pressure in capillaries Renal blood flow Activation of the reninangiotensinaldehsterone system Albumin Retention of, Kidney failure Blood volume Osmotic plasma pressure Edema

6 Clinical significance of edema Ascites due to liver cirrhosis

7 Clinical significance of edema Pulmonary edema Hydrotorax CAUSES A) cardiac (AH, decreased contractility of the heart, etc.) B) non-cardial (hypervolemia, hypoproteinemia, shock, gas poisoning, etc.)

8 Clinical significance of edema Cerebral edema

9 Clinical significance of edema Elephantiasis Bancroft's filaria

10 loss of more than 22% is fatal Dehydration (Exicosis) General Classification by mechanism Local Due to insufficient water intake Due to excess water loss total intracellular Drink excrement intravascular ml urine interstitial Food breathing/ skin

11 Violations of the blood volume Arterial plethora hyperemia is increased blood filling of the tissue due to increased arterial blood flow. It can be general - with an increase in the volume of circulating blood and local arising from local effects of various factors. 1. angioneurotic (neuroparalytic) 2. collateral 3. postischemic 4. hyperemia caused by arteriolovenous fistula 5. inflammatory 6. vacant Causes of general arterial plethora Increased plasma volume (intensive infusion therapy) Erythrocytosis - Primary (erythremia) - Secondary (hypoxic conditions: lung diseases, high altitude, etc.)

12 Violations of the blood volume Venous plethora is increased blood filling of an organ or tissue due to the reduction (difficulty) of the outflow of blood; the blood flow is not changed or reduced. Stagnation of venous blood leads to widening of veins and capillaries, slowing of blood flow in them, to the development of, which is the main pathogenetic factor determining changes in organs with venous plethora. acute local chronic general

13 Violations of the blood volume General acute venous plethora General acute venous plethora is occurs with acute heart failure. CAUSES: myocardial infarction, acute myocarditis, cardiac tamponade (and other causes leading to a acute weakening of the contractility of the heart) Due to hypoxia and increased hydrostatic pressure, capillary permeability rises acute, plasma steepness and edema, stasis in capillaries and multiple diapedemic hemorrhages develops in the stroma of the organs; in the parenchyma - dystrophic and necrotic changes. Left ventricle Right ventricle

14 General acute venous plethora Lungs: Edema, Hemorrhage. Acute pulmonary edema is one of the main causes of death of patients with acute cardiovascular insufficiency. Kidney: Dystrophy, Necrosis of the tubular epithelium. Liver: Centrolobular hemorrhages, Necrosis.

15 2. Violations of the blood volume General chronic venous plethora (congestion) A general chronic venous plethora occurs with chronic cardiovascular failure (coronary heart disease, chronic myocarditis, cardiomyopathy, heart disease). Prolonged tissue hypoxia leads not only to plasmorrhage, edema, stasis and hemorrhages, dystrophy and necrosis, but also to atrophy and sclerosis (proliferation of connective tissue): stagnant consolidation (induration) of organs and tissues develops. skin serous cavities spleen kidneys lungs liver - Anasarca -Hydrotorax -Hydropericardium -Ascites - Cyanotic induration - Cyanotic induration - Brown induration - Nutmeg liver

16 spleen 2. Violations of the blood volume General chronic venous plethora (congestion) kidneys

17 2. Violations of the blood volume General chronic venous plethora (congestion) lungs

18 2. Violations of the blood volume General chronic venous plethora (congestion) Nutmeg liver

19 Local venous plethora Occurs when the outflow of venous blood from the body or part of the body in connection with closure of the lumen of the vein (thrombus or embolus) or squeezing it from the outside (swelling, expanding tissue). In the organs, the same changes occur as with a common plethora. Muscat liver and nutmeg cirrhosis may occur with thrombophlebitis of the hepatic veins (Badd-Chiari syndrome).

20 2. Violations of the blood volume Ischemia (local anemia) is decrease in the blood filling of the tissue, organ, part of the body as a result of insufficient blood flow. Tissue changes that occur with anemia are due to the duration of the hypoxia that occurs. With acute anemia, dystrophic and necrotic changes usually occur. With chronic anemia, there are atrophy of parenchymal elements and sclerosis of the stroma. spastic obturating compression due to repartition

21 3. Bleeding and hemorrhage Bleeding is the process of the discharge of blood from the lumen of a blood vessel or cavities of the heart into the environment or into the body cavity, as well as interstitial. OUTER INTERNAL PRIMARY SECONDARY Hemorrhage (hematoma) is a kind of internal bleeding with a accumulation of blood in tissues. A special type of hemorrhage - apoplexy - is a rapidly developing massive hemorrhage.

22 Classification of hematomas * * also distinguish uniform hemorrhagic impregnation of the tissue petechiae 1-2 mm CAUSES: AH (1), impaired number and function of platelets (2) purpura 3 mm - 1 cm CAUSES: trauma, vasculitis ecchymosis more than 1 cm CAUSES: injury hematoma in cavities hemothorax hemopericardium hemoperitoneum hemarthrosis hemocephalia

23 Mechanisms of bleeding per rhexin due to rupture CAUSES: trauma inflammation necrosis aneurysm developmental vascular malformations sclerosis hyalinosis per diabrosin due to corroding CAUSES: cancer necrosis inflammation ectopic pregnancy per diapedesis due to impregnation CAUSES: hypoxia intoxication hemorrhagic diathesis

24 Bleeding due to rupture per rhexin

25 Bleeding due to corroding per diabrosin

26 Bleeding due to impregnation per diapedesis

27 Outcome of hematoma The formation of a "rusty" cyst (accumulation of hemosiderin) Encapsulation or fibrosis of the hematoma Suppuration with infection

28 Plasmorrhagia Plasmorrhagia - the exit of plasma from the bloodstream due to increased vascular permeability. It occurs as a result of neuro-vascular disorders (spasm), tissue hypoxia, immunopathological reactions Diseases with plasmorrhagia: hypertensive disease, atherosclerosis, decompensated cardiac defects, infectious, infectious-allergic and autoimmune diseases Outcome fibrinoid necrosis and hyalinosis Plasmorrhagia is important pathophysiological factor in burn disease

29 Blood stasis Stasis of blood - a sharp slowing and stopping the flow of blood in the vessels of the microcirculation Causes of stasis: Infection, Intoxication, Venous plethora, Shock Of great importance is the sludge-phenomenon, for which characteristic is the adherence of red blood cells to each other, leukocytes and platelets and a build-up of viscosity plasma, which leads to difficulty in blood perfusion through the vessels of the microcirculatory bed.

30 Blood Stasis Stasis in the capillaries of the brain: Capillaries and venules are sharply expanded, Overfilled by columns of erythrocytes in the form of coins Swelling of the brain substance. Prolonged stasis in the brain leads to development focal necrosis; clinically it manifests with brain coma.

31 4. Thrombosis A thrombosis is an intravital coagulation of blood in vessels or cavities of the heart with the formation of fibrin. Internal pathway Blood coagulation occurs in 4 stages: 1. thromboplastinogen + activators active thromboplastin. 2. prothrombin + Ca2 + + thromboplastin thrombin. kallikrein prekallikrein Thrombin (IIa) Thrombin (IIa) highmolecular weight kininogen, collagen Outer pathway Tissue destruction Tissue factor (thromboplastin) Tissue factor 3. fibrinogen + thrombin fibrin monomer. Thrombin (IIa) prothrombin thrombin 4. fibrin monomer + fibrin-stimulating factor fibrin polymer. Phospholipid surface Active factor Non-active factor Common pathway fibrinogen fibrin fibrin polymer

32 endothelium basal membrane smooth muscle of an arteriola Primary hemostasis Destruction site platelet shape change Platelet adhesion von Willebrand factor ADP, TxA2 granule release platelet mobilization Adhesion and formation of a hemostatic plug release of endothelin causes vasoconstriction reflex vasoconstriction collagen endothelium B basal membrane collagen Secondary hemostasis Thrombosis and angiotembotic events Expression of the phospholipid complex Tissue factor Thrombin activation Fibrin polymerization Tissue factor Release of - t-pa (fibrinolysis) - Thrombomodulin (coagulation cascade blocking) Captured neutrophils Captured erythrocytes Polymerized fibrin C fibrin D

33 Thrombosis factors: General: Changes in the vascular wall Slowing and disturbing blood flow Local: Misbalance between coagulation and anticoagulation systems of blood Violation of rheological properties of blood (increased viscosity).

34

35 4. Thrombosis Classification of thrombi by morphological features (by color, composition) RED Erythrocytes + fibrin + platelets WHITE Platelets + fibrin In the veins In large arteries COMPOSITE Layered Veins, aortic aneurysm, chambers of the heart HYALINE Destroyed erythrocytes, plasma proteins Microcirculatory bed

36 4. Thrombosis Classification of thrombi In relation to the lumen of the vessel: 1. Parietal - lying at the wall of the vessel, thus there is a free part of the lumen. 2. Obturating or occluding the lumen of the vessel. 3. Axial, freely lying in the lumen of the vessel or cavity of the heart. According to the shape: 1. Elongated thrombi. 2. Spherical thrombi in the cavities of the heart or in the saccular aneurysm. 3. Small blood clots resembling beads, the so-called "warts". They are often found on valve flaps.

37 Thrombosis: structure of composite thrombus 1. head (has the structure of a white clot), attached to the vascular wall; 2. body (actually mixed thrombus); 1 3. tail (has the structure of a red blood clot). 3 3

38 Thrombus vs post-mortem blood clot Thrombus Criteria Postmortem clot Dark-red Color White-red Dry Consistency Elastic Rough, dim Surface Smooth, glance Attached with head In relation to vascular wall Free lying

39 Thrombus vs post-mortem blood clot Zahn lines in trombus on cut

40 Outcomes of thrombosis FAVORABLE: Aseptic autolysis (dissolution of a blood clot) Organization of a thrombus, that is, the replacement of a thrombus with a connective tissue that grows from the side of the intima; The process can be accompanied by recanalization and vascularization. Calcification (in the veins, there are stones - phlebolites) ADVERSE: Septic autolysis with the development of septicopyemia Disengage the thrombus with the development of thromboembolic events Progression Clinical significance: thrombosis - > ischemia - > infarction and gangrenes thrombosis - > thromboembolism - > infarction and gangrenes

41 Embolism Embolism - circulation in the blood (or lymph) not occurring under normal conditions particle with blockage of vessels Such particles are called embolus (emboli)

42 Embolism classification Depending on the direction of embolus movement: Orthograde embolism with blood flow, Retrograde embolism - against blood flow, Paradoxical embolism - embolus from the veins of a large circle, bypassing the lungs, enters the arteries of a large circle (through defects in the septa of the heart). Depending on the nature of the emboli: Thromboembolism (venous and arterial), Fat embolism, Air embolism, Gas embolism, Tissue (cellular) embolism (+Amniotic fluid embolism) Microbial embolism, Embolism with foreign bodies

43 Venous embolism: pulmonary embolism (PE) Source: thrombi of the veins of the lower limbs, veins of the pelvic floor, arising with venous stasis, as well as thrombi of the right heart chambers In the genesis of death in PE, closure of the lumen of the vessel with the development of acute right ventricular failure, as well as pulmonary-coronary reflex (Kitaev s reflex): spasm of the bronchi, branches of the pulmonary artery and coronary arteries Outcomes: Heart arrest and death Hemorrhagic lung infarction

44 2-4 cases per 1000 hospitalizations (USA) 95% - source of thrombus - veins of lower extremities (above the knee joint)

45 Arterial embolism Source: thrombi formed in left heart chambers (with endocarditis, heart defects, myocardial infarction, arrhythmia, etc.) and in the aorta (or large arteries) atherosclerosis Outcomes: Ischemic infarctions and gangrenes in organs

46 Thromboembolic syndrome = systemic thrombosis Includes: Thrombosis Multiple arterial thromboembolism Infartion of gangrene (brain 10%, lower limbs 75%, other 10%) Causes Cardiovascular diseases, Oncological diseases, Infectious (sepsis) diseases, Postoperative period.

47 Fat embolism Develops when drops of fat enter the bloodstream: In case of traumatic bone marrow injury (fractures of long tubular bones), Crushing subcutaneous fat, After intravenous administration of oil solutions. Fat drops obturate capillaries of the lungs and through arteriovenous anastomoses enter a large circle blood circulation, obturate the capillaries of the kidneys, brain and other organ Fat droplets can be revealed by sudan III staining in interalveolar septae capillaries Outcomes: acute pulmonary insufficiency, brain capillaries obturation with multiple brain hemorrhages

48 Fat embolism

49 Air embolism Develops air enters the bloodstream: After the wounds of the veins of the neck (negative pressure) After childbirth and abortion, through the sclerotized lung, with occasional intravenous injection air together with the drug substance. Air bubbles in the blood cause embolism of capillaries of a lung; when air bubbles reach a large circle blood circulation embolism of capillaries the brain can develop. Air embolism can be detected on the autopsy by release of air from the right heart after puncturing it underwater and a foamy blood in the cavities of the heart.

50 Air embolism test

51 Gas embolism Typical for caisson disease=decompression sickness: develops with rapid decompression (transfer from increased pressure to normal atmospheric pressure or from normal to decreased). Released nitrogen bubbles (located at high blood pressure in the dissolved state) cause blockage of the brain and spinal cord, liver, kidneys and other body s parts capillaries, which is accompanied by the appearance in them small foci of ischemia and necrosis.

52 Tissue embolism May occur when tissue is destroyed due to trauma or pathological process leading to the inflow of pieces of tissue (cells) into the blood. Embolism of amniotic fluid in woman in labor may be accompanied by the development of DIC syndrome and lead to death. Embolism of malignant tumor cells lies in the tumor metastasis: in organs numerous tumor nodes round in shape are revealed, often with a dip in the center (necrosis).

53 Tissue embolism (cancer cells)

54 Microbial embolism Bacteria, fungi, protozoa circulate in the blood and obturate the capillaries lumen. Often, bacterial emboli are formed in purulent melting of thrombus - thrombobacterial embolism. At the site of occlusion of the vessel with bacterial emboli formed metastatic abscesses. An example of bacterial embolism may embolic purulent nephritis (often found in septicopyemia): The kidney is enlarged in size, Cortex and medulla show multiple small yellowish foci (purulent inflammation).

55 Foreign bodies embolism Catheters, bullets, as well as crystals of cholesterol from ulcerating atherosclerotic plaques

56 Shock Shock - circulatory collapse, accompanied by hypoperfusion of tissues and decrease in their oxygenation.

57 Shock morphology Kidney: Necrotizing nephrosis (acute renal failure) Lungs: Adult Respiratory Distress Syndrome (ARDS). Foci of atelectasis, Serous hemorrhagic edema with accumulation of fibrin in lumen of the alveoli (hyaline membranes), Stasis and thrombi in microcirculatory bed. Liver: Centrolobular necrosis. Brain: Foci of necrosis, Minor hemorrhages. Gastrointestinal tract: Hemorrhages.

58 Disseminated intravascular blood coagulation syndrome (DIC) The syndrome of disseminated intravascular coagulation of blood (coagulopathy of consumption, thrombohemorrhagic syndrome) - a condition, characterized by the formation of multiple blood clots in the vessels of the microvasculature due to the activation of coagulation factors and developing deficit with subsequent activation of fibrinolysis and development of numerous hemorrhages.

59 Stages of DIC Stage I - hypercoagulation and thrombus formation: It is characterized by intravascular aggregation of blood cells, disseminated blood coagulation with the formation of multiple blood clots in microvessels of various organs and tissues. As a rule, it is short-term, duration up to 8-10 min. Clinically manifests as a shock. Stage II - increasing coagulopathy of consumption: Characterized by a significant decreased amountof platelets and fibrinogen, spent on the formation of thrombi. There is a transition from hyper- to hypocoagulation, manifesting by hemorrhagic syndrome. Removal of active coagulation factors from the blood stream is due to phagocytosis, so the presence of fibrin in cytoplasm of macrophages and neutrophils is confirmation of this stage.

60 Stages of DIC Stage III - pronounced hypocoagulation and activation fibinolysis: There is a lysis of previously formed microthrombi and often the degradation of circulating clot factors Developing hyperplasminemia leads to the appearance of readily soluble and fibrin-containing complexes, fibrin degradation products, and fibrin-monomer looses its ability to polymerize. It usually develops 2 to 8 hours after the onset of DIC. Complete blood incoagulability, severe bleeding and hemorrhage, microangiopathic hemolytic anemia are noted.

61 Stages of DIC Stage IV - Restorative (residual manifestations): Dystrophic, necrotic and hemorrhagic lesions of organs and tissues. In most cases, there is a reverse development of tissue changes. In severe cases of DIC syndrome, lethality is 50% due to acute polyorganic insufficiency. In newborns, especially premature born, mortality is 75-90% (due to imperfect fibrinolytic system, insufficient synthesis of liver clotting factors, etc.)

62 Morphology of DIC Morphology and morphogenesis of DIC syndrome are due to a number of factors, among which an important role play: The main disease, DIC triggering mechanisms, Time, Treatment measures Regardless of the combination of these factors, the main morphological manifestations of DIC syndrome are: Microthrombi, Necrosis, Hemorrhages.

63 Morphology of DIC Multiple microthrombi in the vessels of microcirculatory bed: Fibrin clots: Detected most often and in the largest quantity. Consist of fibrin with single red blood cells. Hyaline thrombi, White (leukocytic) thrombi, Red (erythrocyte) blood clots.

64 Morphology of DIC Lungs: Serous-hemorrhagic edema, Fibrin and hyaline thrombi, Sludge and agglutination of erythrocytes, Multiple hemorrhages, Small hemorrhagic infarctions (in some cases), Hyaline membranes (consisting of fibrin). Pancreas: Edema, Hemorrhages, Microthrombi, In severe cases, pancreatic necrosis.

65 Morphology of DIC Kidney: Dystrophy of the proximal and distal convoluted tubules epithelium, In severe cases, necrotic nephrosis (necrosis tubular epithelium, tubulorhexis, symmetrical focal and total corticonecrosis), Multiple hemorrhages, incl. subcapsular, Multiple microtrombi. Liver: Dystrophic and necrotic changes in hepatocytes (up to centrolobular necrosis), Fibrin thrombi in the central veins, filaments of fibrin lying freely in sinusoids.

66 Shock kidney

67 Shock liver

68 Morphology of DIC Adrenal glands: Dystrophy with loss of lipids and necrosis of cells in cortex and medulla, Multiple microthrombi, Extensive hemorrhage (Waterhouse Friderixen syndrome). Skin: Multiple petechial hemorrhages, Rarely - extensive hemorrhages (ecchymosis), Small necrotic foci (in some cases). Gastrointestinal tract: Multiple small hemorrhages, Erosions and acute ulcers.

69 Morphology of DIC Spleen Small-scale hemorrhages in parenchyma and capsule Hyaline and fibrin thrombi in small arteries and veins Fibrin fibers in sinusoids Myocardium and brain (rarely affected) Single microtrombi Dystrophic changes Edema