circulatory disturbance 1 l pathology revision for dental student

circulatory disturbance 1 ( the definition , cause , pathology , types of hyperemia and thrombosis with fate of it)  l pathology revision for dental student

 

CIRCULATORY DISTURBANCES

Active Hyperaemia

• Increase in the blood flow to an organ as a result of active dilatation of its arterioles and capillaries. Active means change in the muscle tone of the vessels.

Types:

• Physiological: e.g. in muscular exercise.
• Pathological :e.g. in acute inflammation.

VENOUS CONGESTION (Passive Hyperaemia)

• Increase venous blood in an organ as a result of obstruction to the venous outflow. The veins, venules and capillaries in the organ become passively dilated.

Types:

• General: Which may be acute or chronic.
• Local: Which may be acute or chronic.

GENERAL VENOUS CONGESTION

• Acute General Venous Congestion

• Terminal condition in acute heart failure. All viscera show acute congestion.

• Chronic General Venous Congestion
• Gradual venous congestion affecting the whole venous system.
• Causes: It is caused by right sided heart failure due to chronic obstructive lesions affecting:

1. The heart: As mitral stenosis and myocardial fibrosis caused by coronary atherosclerosis.
2. The pulmonary vessels: As congenital pulmonary stenosis and bilharziasis of the lung which causes narrowing of the pulmonary arterioles.
3. The lung: As emphysema and extensive fibrosis caused by tuberculosis and pneumoconiosis.

General Effects:

• Dyspnea.
• Cyanosis ; Caused by: Stasis in the capillaries causes more hemoglobin reduction by the tissues and Deficient oxygen saturation in the congested lung.
• Cardiac edema: edema caused by right sided heart failure.
• Causes:

1. Increased hydrostatic pressure in the veins and capillaries caused by the congestion.
2. Increased capillary permeability caused by the anoxia.
3. Venous congestion in the kidney causes sodium and water retention.

• Sites:
• edema begins around the ankle because of the effect of gravity. Later it spreads upwards and becomes generalized "anasarca" and associated with ascitis, hydrothorax and hydro pericardium.
• Characters of edema:
• The edema is pitting. The edema fluid has a protein content below 3 gm%, a specific gravity below 1015 and it does not clot on standing.

Local Effects:

Heart:

• In case of mitral stenosis the left atrium becomes distended by blood. Next the pulmonary veins and capillaries are distended. Lastly the back pressure is reflected on the right side of the heart and all systemic veins with their dilatation.

Lung: The lung is affected in right sided heart failure caused by mitral stenosis and in left sided heart failure.

• Gross picture:
• The lungs are enlarged, heavy, firm and dark red. The cut surface exudes blood stained fluid. The bronchial mucosa is congested and covered by a viscid layer of brownish mucus.
• Microscopic picture:

1. The alveolar capillaries are dilated and congested. The increased pressure causes rupture of some of the capillaries and hemorrhage occurs in the alveolar spaces.
2. The extravasated red cells hemolysis and liberate hemoglobin with release of hemosiderin. Hemosiderin and the red cells are removed by macrophages which appear swollen and brown and are called heart failure cells.
3. Some of these cells return back to the interstitial tissue in their way to the draining lymph node. Some of them die and the released hemosiderin causes fibrosis in the interstitial tissue of the lung. The lung becomes brown and tough, a condition called brown induration.
4. Homogenous pink transudate appears in the alveoli and the interstitial tissues. The transudate is marked in the basal and posterior parts of the lung due to the effect of gravity.

• Clinically:
• Chronic cough and hemoptysis.

Liver:

• Gross picture: The liver is enlarged heavy and firm. The capsule is tense. The cut surface shows alteration of brown(congested)and yellow(fatty change) coloration. The appearance is called nutmeg liver.

• Microscopic picture: The central veins and central ends of the sinusoids appear dilated and congested. The liver cells in the center of each lobule undergo degeneration and necrosis as a result of pressure by the congested sinusoids and anoxaemia. The cells at the periphery of the lobules are less affected and show fatty change. Hemosiderin granules appear in Kupffer cells. In advanced cases cardiac cirrhosis occurs

• Clinically: Enlarged, tender liver.

Spleen:

• Gross picture: The spleen is enlarged, heavy and firm. The edges are sharp. The capsule is thick. The cut surface is dark red.

• Microscopic picture: The venous sinuses are distended with red cells and contain many macrophages loaded with hemosiderin. The littoral cells show phagocytic activity. The lymphoid follicles show pressure atrophy.

Kidney:

• Gross picture: The kidney is slightly enlarged, firm, dark red and dripples blood on cutting. The cut surface shows dark red dots(congested glomeruli) and dark red streaks(congested vessels).

• Microscopic picture: The glomerular capillaries and medullary veins are congested. Red cells and pink transudate appear in the Bowman's space and in the tubules.

• Clinically: Hematuria and albuminuria.

Stomach and Intestine:

The mucosa is congested, swollen and covered by viscid brown mucus.

LOCAL VENOUS CONGESTION

• Localized congestion in any part of the body whose venous outflow becomes obstructed.

Acute Local Venous Congestion

• Causes: Sudden complete venous obstruction due to thrombosis. ligature or twisting of the pedicle of a movable organ or strangulated hernia.

• Pathology: Rapid severe distention of the veins and capillaries which may rupture. edema occurs rapidly in the tissues.

Chronic Local Venous Congestion

• Causes:  Gradual incomplete venous obstruction. It results from venous compression by a tumor, enlarged lymph node or pregnant uterus. Also it results from liver cirrhosis and bilharzial hepatic fibrosis.

• Pathology: The veins, venules and capillaries proximal to the obstruction become dilated and congested resulting in edema. Gradual opening of the collateral and anastomotic veins.

Examples of Chronic Local Venous Congestion:

•  Compression of the femoral vein: Causes venous congestion, swelling. edema and cyanosis of the lower limb.

•  Liver cirrhosis or fibrosis: Causes obstruction of the hepatic veins with the following results:

1. Venous congestion in the portal area.

2. Ascitis.

3. Splenomegaly.

4. Opening of the anastomosis between the portal and systemic veins causing esophageal varices and hemorrhoids.

THROMBOSIS

• Formation of a compact mass composed of the elements of the circulating blood inside a vessel or a heart cavity during life. This compact mass is called thrombus.

Causes of Thrombosis:

• Damage to The Vascular Endothelium:

•  Mechanical e.g. trauma, pressure and ligature.
• Inflammatory e.g. phlebitis, arteritis and endocarditis.
• Degenerative e.g. atheroma, aneurysm and myocardial infarction.
• The platelet adhere to the damaged endothelium.

• Slowing of Blood Stream (Stasis): 

• In normal blood stream, the blood cells occupy the central part and the plasma the peripheral part. In stasis, the platelets cross the plasmatic zone and come in contact to the vascular endothelium. Slowing occurs in the following conditions:
• In heart failure specially in the leg veins.
• In the auricles of the heart in association with valvular diseases.
• In aneurysmal sacs, varicose veins and in the portal vein secondary to liver cirrhosis.
• In tissues showing acute inflammation.

• Disorders of Blood Stream: 

• Distortion of the vascular lumen as in aneurysm, atheroma, varicose veins and compression of the vessel wall from outside allows the platelets to come in contact with the vascular endothelium thus initiating thrombosis.

• Changes in Blood Composition:

• Platelets: After operations the platelets increase in number and become more sticky. They agglutinate in small masses and adhere to the vascular endothelium. Their lysis release thromboplastin which starts thrombosis.
• Fibrinogen: Increases during pregnancy and in lobar pneumonia.
• Red cells: Increase in polycythemia causing increased blood viscosity and stasis.
• White blood cells: Increase in leukemia causing increased viscosity and stasis.
• Plasma: Decreased plasma volume as in dehydration.

• More than one of the above factors may be the cause of thrombosis.

 

Mode of Formation and Types of Thrombi:

Pale thrombus (platelet thrombus):

• The initial thrombus is composed of platelets only. The platelets deposit on the site of endothelial damage. They adhere to the exposed sub endothelial collagen by the help of Von Willebrand factor(factor VIII).

• This factor is produced by endothelial cells and acts as a bridge between platelet surface receptors and collagen.

• The adherent platelets release adenosine diphosphate(ADP) and serotonin which promote further aggregation and adhesion of platelets forming a small white amorphous mass.

• Such platelet thrombus is fragile and can be washed away by the blood stream except if stasis is present.

Mixed thrombus:

• Stasis allows clotting factors to accumulate in the area. Thromboplastin released from the platelets and damaged tissue promotes fibrin formation which deposits on the primary platelet thrombus.

• Next the deposited fibrin encourages further platelet accumulation. The platelets deposit as laminae at right angle to the blood stream.

• Between the laminae there is complete blood stasis and fibrin is deposited entangling the red and white blood cells.

• The formed thrombus is a mixed one as it is composed of both platelet masses and blood clots. In paraffin section it shows alternate layers of fused platelets, and fibrin with entrapped blood cells.

• The fused platelets appear as homogenous reddish violet streaks called lines of Zahn. If the resulting thrombus occludes the vessel partially it is called mural thrombus.

• If the thrombus occludes the vessel completely it is called occluding thrombus.

Propagating thrombus:

• If the formed thrombus occludes a vein completely, proximal to occlusion the blood will be stagnant and it clots.

• The clot is soft, red and fixed to the original thrombus but not to the vascular wall.

• When this propagating thrombus reaches a level at which a tributary or a branch joins the affected vein, thrombosis starts again as the blood once more will be in motion (thrombosis occurs in moving blood, clotting in stagnant blood).

• The process can be repeated and the propagating thrombus extends in the direction of the heart.

Classification of Thrombi:

• Thrombi are classified according to the color and the presence or absence of bacteria.

Color:

1. Pale thrombus: Formed mainly of platelets and fibrin. It is small, greyish white, firm and adherent to the intima e.g. cardiac vegetation.

2. Red thrombus: Formed mainly of red cells and fibrin. It is dark red, soft and loosely attached to the vessel wall. It is very rare.

3. Mixed thrombus: Most thrombi has pale and red components.

Presence or Absence of Bacteria:

1. Infected thrombus: The thrombus contains bacteria. If the bacteria are pyogenic the thrombus is called septic thrombus.

2. Non infected thrombus (aseptic): It contains no bacteria.

Sites of Thrombus Formation:

Thrombosis in Veins:

• More common because of their slow blood flow and thin wall. Two types occur:

• Thrombophlebitis: Thrombosis is initiated by inflammation of the venous wall. Two types occur:

1. Septic thrombophlebitis: Occurs in veins draining septic lesions as in appendicular vein in case of acute appendicitis and in pelvic veins in case of puerperal sepsis.
2. Aseptic thrombophlebitis: Inflammation is caused by factors other than bacteria as trauma and radiations. A small fixed aseptic thrombus occurs.
• Phlebothrombosis: Thrombosis caused by factors other than inflammation e.g.: Occurs in the veins of the feet and calf in chronic cardiac patients confined to bed due to:
1. Stasis caused by the heart lesion and the absence of muscular movements.
2. Compression of the calf muscles against the bed mattress. The thrombus may propagate to the femoral and iliac veins and may fragment causing pulmonary embolism.
3. In the femoral and pelvic veins after labor or abdominal operations.

• The factors responsible are:

1. Platelets increase in number and become more sticky.
2. Prolonged bed rest leads to stasis.
3. Mild inflammation at the operation site.
4. Thrombosis in varicose veins due to stasis.

Thrombosis in Arteries:

• Less common than venous thrombosis because of the rapid blood flow in the arteries and the thick elastic arterial wall which resists injury. Thrombosis occurs in arteries affected by:

1. Atheroma, polyarthritis nodosa, thromboangitis obliterans due to roughness of the intima.

2. Aneurysms due to stasis, disordered blood stream and roughness of the intima.

• Arterial thrombosis causes ischemia.

Thrombosis in the Heart:

• More common in the left side. The following types occur:

1. Mural thrombi: Occur over infarcts, commonly on the endocardial surface of the left ventricle near the apex.

2. Vegetations:Pale thrombi over the valves in rheumatic and bacterial endocarditis.

3. Auricular thrombi: Develop in the atrial appendages in heart failure due to stasis. Commonly in the left auricle in mitral stenosis. They are commonly adherent to the wall. Rarely the thrombus detach and remains in the dilated atrial cavity and is called ball thrombus.

4. Agonal thrombi: Red thrombi occurring in the ventricles commonly the right at the time of death specially caused by lobar pneumonia.

Thrombosis in Capillaries:

• Capillary thrombosis rarely occurs in acute inflammation, severe cold and frost bite. They are due to stasis. endothelial damage and haemoconcentration.

Fate of the Thrombus:

• Septic Thrombus: Fragments by the proteolytic enzymes into septic emboli causing pyaemic abscesses.

• Aseptic Thrombus: Its elements disintegrate and form a pale red structureless mass. If the mass is small it dissolves by fibrinolysis. If the mass is large it undergoes:

1. Organization: The thrombus is invaded by capillaries and fibroblasts from the vascular wall and change to a fibrous mass. This causes permanent vascular occlusion.

2. Organization and canalization: Occasionally some of the capillaries dilate and allow passage of blood through the thrombus or the fibrosed thrombus shrinks from the vascular wall leaving a space which gets lined by endothelium.

3. Dystrophic calcification: May occur giving a phlebolith.

4. Detachment: Forming aseptic emboli causing infarcts.

5. Propagating thrombus: Due to spread of venous thrombosis.

Clot:

• A mass of blood elements formed in stagnant blood. The clot is soft, dark red with a glistening smooth surface. The clot is not adherent to the vessel wall.

Post-mortem clots:

• Occur in the cardiac chambers after death. There are two types:

1. Red or current jelly clot: Occurs with rapid blood clotting. It is formed of a fibrin network entangling red and white blood cells.

2. Yellow or chicken fat clot: Occurs with slow blood clotting. This allows sedimentation of the red cells in the dependent part with plasma, fibrin and white cells above. Slow clotting occurs with anticoagulant therapy or with deficient coagulation factors as in haemophilia.