HEMODYNAMIC DISORDERS VASCULAR PATHOLOGY
I/Introduction
II/Blood stasis
1. Edema
2. Congestion
2.1 Active congestion
2. 2 Passive congestion
3. Hemorrhage
III/Thrombosis and thromboembolic diseases
1. Thrombosis
2. Embolism
3. Ischemia
4. Heart attack
Introduction :
The nutrition and functioning of cells and tissues require normal blood, lymphatic and interstitial circulation.
Exchanges between blood and tissues require a balance ensured by:
- Intravascular pressures: Hydrostatic which tends to force plasma constituents out and Oncotic which tends to retain these constituents in the vessels
- Integrity of the vascular lumen
- Integrity of the vascular wall
I/ Blood stasis and hemodynamic pathology
A/ Tissue edema:
- Definition: It is an increase in the amount of water in the extravascular spaces.
- Macroscopic appearance: the edematous tissues and organs are soft and pale: after incision, they may leak a slightly pink liquid. Edemas predominate in the dependent parts (gingival edemas). The tissue sometimes retains the imprint of the finger when pressed (pit sign). Edema may affect the natural cavities of the body: serous (pleural effusion, ascites), joint cavities (hydarthrosis). Anasarca refers to generalized edema.
- Microscopic appearance : microscopic abnormalities are quite subtle to identify. The tissue is infiltrated by a pale, very weakly eosinophilic serosity, separating the normal constituent elements (cells, fibers) from each other.
- Pathophysiology : There are two types of edema:
– hemodynamic edema or transudates poor in plasma proteins and resulting from several mechanisms:
*increased hydrostatic pressure in the venous system: for example generalized edema due to congestive heart failure.
* decrease in oncotic pressure of plasma proteins: in hypoproteinemia
* hydro-sodium retention: renal failure…
– lesional edema or exudates rich in plasma proteins and due to an increase in endothelial permeability (initial phase of inflammation).
- Consequences: variable depending on the location and intensity of the edema
– possible sudden death (acute glottis edema, APO: acute pulmonary edema).
– compression hindering the functioning of an organ (ventricular function disorders during hydropericardium (tamponade).
-inflammatory reaction (and superinfection): prolonged edema.
B/Vascular congestion
- Definition : It is an increase in the quantity of blood contained in vessels which dilate.
- Macroscopy: organ heavy, red.
- Microscopy: the vessels are dilated, filled with red blood cells, with cells
turgid endothelial cells.
Two types are recognized:
Active congestion by influx of arterial blood (Hyperemia) by active vasodilation of the microcirculation: local redness and heat, increased weight of organs.
She observes herself:
-by reflex nervous mechanism,
-by adaptation during increased functional demand (muscle in exercise),
– during the initial phase of inflammation through the use of chemical mediators.
Passive congestion is the consequence of a slowing of venous blood drainage (stasis).
It is accompanied by passive dilation of the veins and capillaries and a decrease in blood flow. The tissues suffer from hypoxia: the endothelial cells are the first to be altered, which, associated with a local increase in hydrostatic pressure, produces edema. The organs are cold, purplish blue (= cyanosis due to desaturation of hemoglobin), and of increased weight.
Passive congestion can be localized , of venous origin, linked to stasis, obliteration (thrombosis) or venous compression.
It can also be generalized , due to heart failure. The consequences are different depending on the type of heart failure.
C/Hemorrhages:
- Definition: Eruption of blood outside the vessels.
– arterial hemorrhage: bright red blood flowing in jerky patterns
– venous hemorrhage: dark red blood flowing continuously
– capillary hemorrhage: in sheets
- Anatomical types:
-External: hematemesis, rectal bleeding, epistaxis, hemoptysis, gingival bleeding.
-Collected in a natural cavity (hemothorax, hemopericardium, hemoperitoneum, hemosalpinx).
-Intra-tissue: hematoma, interstitial hemorrhages (ecchymosis, purpura, petechiae).
- Etiologies
Multiple circumstances:
– rupture of vessels (traumatic, ischemic or pathological necrosis, etc.)
– erythrodiapedes: water passes through altered capillary walls: lesions of the endothelium by bacterial toxins (in septicemia, etc.).
- Anatomo-clinical aspects:
Macroscopy
- varies depending on importance, size and location
- Visible on the surface of skin, oral cavity, viscera, brain
- Does not fade under pressure
petechiae (1-2 mm)
purpura (3mm to 1cm)
bruising (extensive ill-defined areas)
Hematoma ( very limited collection)
Blood effusions in natural cavities ( Hemopericardium, Hemoperitoneum, Hemarthosis )
Hemoptysis/Hematemesis
Microscopy
• Extravasated red blood cells in the tissues
• Hb released by the destruction of red blood cells disintegrates
– in ferric derivatives: hemosiderin, hemofuscin
– Pigment derivatives: bilirubin and porphyrin
- Evolution of localized hemorrhages
∙ Small tissue hemorrhages gradually progress to resorption and
healing, with inflammatory reaction and local degradation of hemoglobin:
hemosiderin and other heme-derived pigments (“local biligeny”, explaining the
successive passage of bruises through different colors). Macrophages are responsible for
hemosiderin pigment (siderophages).
∙ If the hemorrhage, abundant, is accompanied by tissue necrosis: development
of an inflammatory reaction, resulting in fibrous scar tissue tattooed with hemosiderin, sometimes calcified.
∙ In the case of a large hematoma, the debridement is often incomplete: a
encystment, we speak of encysted hematoma . This hematoma is a fibrous shell surrounding degraded blood (citrine liquid, tinged with hemosiderin and containing crystals of
cholesterol). Rarely, superinfection with suppuration may occur.
∙ In a serous cavity, fibrin deposits will organize into fibrous tissue,
thickening the serous membranes and tending to give adhesions or symphyses
(adhesion of the visceral and parietal layers of the serosa).
- Consequences :
– hypovolemic shock in case of heavy and rapid bleeding.
– iron deficiency anemia if the hemorrhages are spaced out over time and slow.
– destruction of vital functioning tissue (intracerebral or adrenal hemorrhage).
– compression hindering functioning: hemopericardium causing a
acute heart failure.
II/ Thrombosis and thromboembolic disease
A/ Thrombosis
- Definition: blood clotting in vivo in a vessel or the heart.
Thrombus = different varieties of coagulation formed during a process
thrombosis, to be differentiated from a clot (= product of blood coagulation in vitro or
after death).
- Training mechanism:
Platelet adhesion-> release->reversible aggregation -> irreversible aggregation.
- Morphology
In its typical form, complete venous thrombus formed after several hours
consists of three parts:
a head: white thrombus made up of platelets and fibrin adhering to the wall.
a body: mixed thrombus made up of alternating blood elements (leukocytes, red blood cells, platelets) and fibrin: striated appearance.
a tail: red thrombus : blood more or less well coagulated with little fibrin floating downstream of the vessel
The thrombus adheres to the wall, obstructing +/- the lumen
- Evolution
– Total lysis and disappearance (possible for small and recent thrombi)
– Organization of the thrombus: most frequent evolution by fibrous transformation
which begins at the 48th hour +/- re-permeabilization
- Complications : liquefaction, suppuration, precipitation of lipid deposits or
calcareous, calcification, migration = migration into the bloodstream
constituting an embolus = main risk of developing thrombosis (rupture is often early in the hours following the formation of the thrombus before its fibrous organization).
B/ Embolisms:
- Definition : Embolism is the circulation of a foreign body (exogenous or endogenous)
in the circulatory current and its stoppage in a vessel too small to deliver it
passage.
- Nature : venous fibrino-cruoric emboli +++ (95%): these are fragments of
thrombi that migrate into the circulation. The most emboligenic thromboses are
thrombosis of the veins of the lower limbs and pelvis, thrombosis
cardiac, thrombosis of arterial aneurysms, arterial thrombosis at
near a fork.
Other emboli:
– gaseous : vascular injury with introduction of air, decompression sickness
– fatty : bone marrow from a fracture site
– atheromatous (called “cholesterol”) : fragment of atherosclerotic plaque
ulcerated
– tumor : aggregate of cancer cells
– foreign body (catheter, etc.)
– parasitic, microbial, amniotic
- Consequences : – Local: endothelial lesion and thrombus
Regional: cessation of blood circulation resulting in ischemia and anoxia if terminal circulation. In case of collateral circulation or red infarction.
- General: null or death
C/ Ischemia:
- Definition: it is the reduction or cessation of arterial blood supply in a territory
limited of the organism.
Causes: These are all the causes of partial or total obliteration of an arterial lumen: atherosclerosis, thrombosis, embolism, arteritis (primary inflammatory disease of the arterial wall), extrinsic compression, arterial dissection, prolonged arterial spasm.
- Consequence : Anoxia = oxygen deficit in the area concerned, hence a
cellular suffering
Factors influencing the impact of ischemia:
– intensity and duration
– tissue sensitivity (neurons very sensitive to ischemia: irreversible lesions after 3 to 5 minutes of anoxia), as well as the myocardium (20 to 30 minutes) and epithelial cells.
– possibility of a replacement circulation, organs naturally rich in anastomoses (stomach, intestine) or provided with a double circulation (lungs, liver) will be more resistant
– speed of installation:
– sudden ischemia does not allow time for a replacement circulation to develop. If it continues, it leads to irreversible cellular damage: tissue necrosis.
– partial, chronic ischemia allows the establishment of a replacement circulation and is responsible for atrophy lesions and progressive fibrosis.
D/Heart attacks:
- Definition: circumscribed focus of ischemic necrosis in an organ due to the complete and sudden interruption of arterial circulation.
- Causes:
Acute arterial occlusion: intrinsic (by thrombosis or embolism), extrinsic from external cause.
There are several types of heart attacks:
White infarction: solid organs with terminal circulation ( spleen, kidney, brain,
Heart, salivary glands) = coagulation necrosis.
Macroscopy
In the first hours the lesion gradually becomes visible. It corresponds to an arterial distribution area (pyramidal shape with peripheral base), paler and softer than the rest of the organ, gradually becoming yellowish white surrounded by a congestive border. During the first weeks the limits of the infarction are increasingly clear, it is surrounded by inflammation. From the third week a whitish fibrous scar forms with thinning and retraction of the injured area.
Microscopy :
No microscopic abnormalities before 6 hours, then appearance between 6 and 48 hours of coagulation necrosis preserving the cellular contours, progressively surrounded and penetrated by an acute inflammatory reaction rich in polymorphonuclear cells.
Then progressive centripetal detersion by macrophages and replacement of the necrotic tissue by a fleshy bud . After one to two weeks, healing begins: connective tissue organization, fibrosis.
Red infarction : concerns hollow organs (such as lung, intestine ) with anastomotic circulation
HEMODYNAMIC DISORDERS VASCULAR PATHOLOGY
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