circulation disorders

Document Sample
circulation disorders Powered By Docstoc
					     Blood circulation disorders
 Normal functioning of a body is possible only in
  condition of normal functioning of blood
  circulation organs, i. e. the heart and vessels.
  Metabolism, oxidation, restoration, enzymatic
  and other processes that are taking place in the
  body cannot be affected without extraction of
  waste products. This transport and metabolic
  function is performed by both blood circulation
  and lymphatic system, which are functioning
 Blood circulatory system coordinates and
  connects functionally different organs and
  systems. This homeostasis coordination
  function is provided by both blood
  circulatory and lymphatic systems.
 Disorders of blood circulation and
  lymphatic circulation occur not only due to
  disturbance in the systems, but also due to
  disorders of heart function and other organs
  at any level.
  Disorders of blood circulation

 1. Disorder of blood supply
 2. Disorders of vascular wall
 3. Disorders of blood flow and its
 Disorders of blood circulation may be
  general, regional, and local in
  character. Such disorders are specific
  not only for pathology: they are
  frequently observed in physiologic
  condition as well, as adaptation or
  particular reflection of a physiologic
 Hyperemia and anemia are related to
  blood-circulation disorders.
 Hyperemia may be:
 arterial
 venous
         Arterial hyperemia

 Arterial hyperemia is a process of
  increased blood supply, as a result of
  larger amount of incoming blood
  and unchanged blood outflow. This
  process is usually local, but it may
  be generalised with an increase of
  circulating blood amount or when
  the number of circulating
  erythrocytes is increased.
 We differentiate:
 angioneurotic           (neuroparalitic,
  vasomotor) arterial hyperemia
 collateral hyperemia
 postanemic hyperemia
 vacate hyperemia
 inflammatory hyperemia
 and hyperemia on the basis of arterio-
  venous fistula
 The signs of arterial hyperemia are
  temperature rise and increase of
  arterial blood pressure.
 The importance of pathologic arterial
  hyperemia is defined by its types and
  is usually insignificant, however
  rupture of a blood vessel may occur.
  Termination of arterial hyperemia
  depends on its time period and
  vascular condition.
          Venous hyperemia

 Venous hyperemia is a process of
  increased blood supply in veins as a
  result of impaired venous outflow.
 We differentiate general and local
  venous hyperemia (plethora).
 Local venous plethora appears as a
  result of impaired blood outflow from
  some organ. General venous plethora
  develops during cardiac
 The signs of venous plethora are
 temperature decrease,
 increase of venous blood pressure,
 cyanosis,
 decrease in organ function.
 Changes in organs in venous
  hyperemia are:
 in the lungs: diapedesis and
  disintegration of erythrocytes happens,
  then hemosiderin is formed from
  hemoglobin. It stains the lungs brown-
  red color, growth of connective tissue
  starts at once (brown induration of the
  lungs). Similar process takes place in
  kidneys and spleen, it leads to organ
Acute local venous plethora in the
 in the liver: venous blood is
  accumulated in central veins (so-called
  nutmeg liver)
«Nutmeg» liver in case of venous
Centrilobular necrosis of liver
 caused by venous plethora

 Anemia (oligohemia, ischemia) is process
  of blood cell amount lowering in the
 We differentiate general and local
 The cause of general anemia is lowering
  of the blood cells amount in the whole
 The causes of local anemia are the
  same as its types. They are:
 angiospastic
 obturational
 compressive
 anemia as result of blood
 The signs of local anemia are:
 pallor
 lowering of blood quantity
 temperature lowering
 decreased function of an organ
 Termination depends on the degree
  of anemia, its time period, its
  temperature, organ functional
  conditions, age. They can be
  insignificant as well as severe,
  including dystrophy and necrosis.
 Prolonged anemia leads to atrophy
  and sclerosis.
Tubular necrosis in ischemia

 Hemorrhage (bleeding) is a process
  of blood outflow from the lumen of a
  blood vessel or the heart. If the
  blood flows into surrounding
  environment, it is external
  hemorrhage. If blood outflows into
  surrounding tissues, it is internal
  hemorrhage. Formation of
  hematoma is result of internal
 Hemorrhage mechanisms are:
 vessel rupture
 ulceration of vascular walls
 bleeding by diapedesis
 Some types of bleeding have their own
 blood spitting - hemoptysis or blood
 bleeding out of the nose - epistaxis or
  nasal bleeding
 blood vomiting - hematenesis or black
 blood excretion with feces - fecal blood
 pathologic bleeding out of the uterus -
  metrorrhagia or uterine bleeding
 Hematoma is the blood that is
  accumulated in tissues outside the
  vascular lumen as result of bleeding.
         Types of hematoma

 Hematoma - hemorrhage with formation
  of a new cavity
 Bruise - hematoma under and flat
 Hemorrhagic infiltration - various
 Petechias and ecchimoses - spot-like
hemorrhages on
surface of
Epidural hematoma
 Hematomas in natural cavities have
  their own terms:
 hemathorax - collection of blood in
  pleural cavity
 hemopericardium - effused blood in
  pericardium cavity
 hemoperitoneum - effused blood in
  peritoneal cavity
 hematocele - effused blood into tunica
  propria testis
 Hematoma outcomes are:
 blood resorbtion
 cyst formation on place of hematoma (as
  in the brain)
 encapsulation
 growth of connective tissue
 infection
 suppuration

 Plasmorrhagia is the process of
  plasma outflow from the vascular
  fed. The result of plasmorrhagia is
  infiltration into vascular wall and of
  the surrounding tissues, that is
  plasmic infiltration. During this
  process the arteriolar walls become
  homogenous and thick. Fibrinoid
  necrosis may develop.
 Importance of plasmorrhagia lies in
  the disturbance of transcapillary
  metabolism and in the structural
  changes in tissues and organs.
 Usually plasmorrhagia is a
  reversible process, but sometimes in
  cases of recurrence or prolonged
  and massive plasmorrhagia fibrinoid
  necrosis and vascular wall
  hyalinization take place.
 Stasis is the process of slowing down or
  total stop of blood circulation in
  microcirculatory vessels.
 Sludge is a phenomenon which is variety
  of stasis. Its main peculiarity is that the
  erythrocytes, thrombocytes or
  leukocytes are agglutinated to each
  other. The increase of blood viscosity is
 Stasis is caused by intoxication,
  infection, venous plethora, vasomotor
  paralysis. The stasis importance is
  defined by its time length, the organ or
  tissue sensitivity to hypoxia. So stasis is a
  reversible process. Prolonged stasis leads
  to thrombosis and necrosis.
Stasis dermatitis is seen here. Years of poor circulation
from poor cardiac function leads to chronic edema and
venous stasis of blood with extravasation of red blood
cells that leads to collection of hemosiderin to give the
skin a brown appearance.
This is a more advanced example of stasis
dermatitis with brownish discoloration from
hemosiderin deposition along with a thickened,
rough appearance to the skin. Ulceration is
possible as well.
 Shock is an acute pathologic process caused
  by strong agents, which is characterized by
  disorder of activity of CNS, metabolism, and
  autoregulation of microcirculatory system,
  which leads to destructive changes in the
  organs and tissues.
 1. Hypovolemic shock - during acute
  decrease of quantity of circulating blood
 2. Traumatic
 3. Cardiogenous
 4. Septic, or toxicoinfectious
   Morphologically, typical signs of shock are:
   hemocoagulation disorders
   hemorrhagic diatesis
   liquid blood in a corpse

 In internal organs there are common changes,
  such as dystrophy and necrosis.
 In shock kidney, the most affected by
  pathologic changes are proximal tubules;
  necrotic nephrosis develops, which causes
  acute renal insufficiency.
 In shock liver develop hydropic dystrophy of
  hepatocytes, centrilobular necrosis.
 When shock changes in kidneys and liver
  combine we speak of hepatorenal syndrome.
Kidneys - necrosis of crimped tubules
 In shock lung develops atelectasis, serous-
  hemorrhagic plethora, formation of thrombi
  in microcirculation vessels, which causes
  development of acute respiratory
 Shock in myocardium is represented by
  necrobiotic changes of cardiomyocytes -
  disappearence of glycogen, appearance of
  lipids, possibly appearance of small zones of
Shock lung
Sludge in myocardium (shock heart)
Shock liver - empty central vein
 For the complete definition of this process we
  have to take into account following issues:
 1. Thrombosis is a process of live blood
  coagulation. Dead blood coagulation isn’t
  called a thrombus but coagulation masses.
 2. Thrombus is a firm mass and may consist
  only of blood cells
 3. Thrombus must be attached to the vascular
  wall; when it is torn off it is called
 So, thrombosis is a process of firm masses
  formation from blood in live person, which is
  attached to the vascular wall.
 Thrombogenesis consists of 4 successive
 1. Thrombocytes agglutination
 2. Fibrinogen coagulation and fibrin
 3. Erythrocytes agglutination
 4. Plasma protein precipitation
 Thrombogenesis may be protective and
  pathologic. This defines the importance of
  thrombosis and its outcome for the body.
 The most frequent localization of a pathologic
  thrombus is:
 veins of the small pelvis (parametral,
  hemorrhoid, vas deferens)
 deep and superficial leg veins
 In relation to the vascular wall thrombus can
  be parietal, that is attached to the vascular
  wall obstructive (occlusive, congestive)
  thrombus. A special form is a ball thrombus.
  It is freely located in the cavity of the left
  atrium and is “polished” by the blood flow.
 The pathogenesis of thrombosis is very
  complicated. We can conventionally
  differentiate local and common factors,
  promoting thrombogenesis.
 The local factors are:
 impairment of vascular wall,
 slowing down of blood flow.
 The common factors are:
 disturbance in regulation of coagulation and
  anticoagulation systems which support the
  liquid state of blood in the vascular lumen
 changes in the blood constituent part
 Termination of thrombosis may be various.
 Local thrombus may undergo aseptic
 vessels may germinate into thrombus (this
  process is called thrombus vascularization)
 thrombus may be replaced by connective
  tissue (thrombus organization)
 shriveling thrombus may acquire cracks
  (thrombus canalization)
 or getting smaller in size it can move away
  from the wall (vascular recanalization)
 Thrombus may be hialinized or calcified. It is
  possible for the thrombus to be torn off and
  turned into an embolus. Also septic lysis of
  the thrombus is possible.
 The importance of such termination is to be
  defined for every patient separately in every
  given situation.
 Clinical importance of pathologic thrombosis
  or thromboembolism is that they have fatal
  complications in many diseases.
Coronary thrombosis
Coronary thrombosis causing ischemia or infarction of
Coronary thrombosis, microscopically
 Embolism is a process of transferring
  particles by blood and lymph flow, which
  are not normally found in the body. These
  particles are called emboli. Often these
  emboli are carried by blood (ortograde
  embolism). Sometimes because of the
  thrombi weight we can observe the
  thrombus moving up the blood flow
  (retrograde embolism) due to gravity.
 Finally, if there is a defect in interatrial or
  interventricular septum, the embolus from
  the veins of systemic circulation occurs in the
  arteries, part of the lungs (paradoxical
  embolism). The emboli may be single and
 The most frequent embolism type is
  thromboembolism, that occurs when the
  thrombus or its part is torn away.
 Fat embolism occurs in the long tubular bone
  fracture or in crushing of the fatty tissue.
 Air embolism occurs when air penetrates into
  the blood.
 Normally there is negative pressure in some
  veins. In pathologic conditions and blood
  losses it is increased (for instance, in uterus
  veins, etc). Accidental introduction of air is
  possible during injections.
 Gas embolism happens during rapid lowering
  of atmospheric pressure (Caisson disease).
 Tissue embolism is brough about during
  traumatic destruction of tissues and due to
  pathologic processes. Tumor cells, pieces of
  heart valves and other particles may become
 Microbial embolism is a frequent process, too.
  It may arise due to microorganisms entering
  the blood vessels or during the thrombus
  septic lysis.
 Embolism with foreign bodies may happen in
  wounds, injuries.
 Special category of embolism is metastatic
  spreading. Metastatic process is a process of
  transference of living particles by the blood or
  lymph flow and formation of the metastasis in
  a new place (the same process as in the
  original place). Malignant tumor cells,
  microorganisms and some parasites
  (echinococcus) may metastasize. The
  metastatic processes have not yet been studied
  completely. There is a great number of
  factors and causes influencing this process.
 The importance of embolism:
 embolism itself may be a complication of
  many diseases and sometimes may be the
  cause of fatal termination.
Large thromboembolus which is deadly for the patient
Thromboembolus in the branch of pulmonary artery,
     Lymph circulation disorders
 Lymph circulation disorders are manifested
  as insufficiency. We differentiate:
 mechanic insufficiency
 dynamic insufficiency
 resorptive insufficiency
 Morphological manifestations of lymph
  circulation disorders do not depend on the
  type of the insufficiency, they are similar.
 The importance and outcome of the lymph
  circulation disorders are defined by the tissue
  metabolic disturbances. Tissue hypoxia is
  developed and then the dystrophic necrobiotic
  processes are observed.

Shared By:
Tags: pathology
Description: Pathologic anatomy subjects