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Transcript
Lecture –5
Dr.Hussein Naji Alshammary
Ass.Prof.Hematology
College of medicine /Babylon university
General pathology /3rd year
Embolism
Embolism: detached intravascular soli, liquid, or gaseous mass that is carried by
the blood flow to a site distant from its point of origin and usually end by tissue
infarction from opbstruction of blood flow.
Classification of Embolism;
A) Physical state:
1. solid: Detached atheroma, detached thrombus, tumor, parasite, bullets, bits of
bone, canula.
2. Liquid: Fat globules, amniotic fluid.
3. Gas: Nitrogen embolism, intravenous injection, fluid and blood transfusion.
Eschemia
Ischemia; Local loss of oxygen supply to the tissue due to parial obstruction of
blood vessels
Causes: 1. Intravascular (intraluminal); Thrombosis, atheroma, embolism.
2. Vascular wall: spasm, vasculitis.
3. extravascular causes: pressure by tumor, Pregnancy, surgical ligature.
Infartion
Area of necrosis caused by complete obstruction of blood flow, arterial or venous.
Type of infarction (morphology):
Red infarction: red color due to presence of hemorrhage (RBC) in the tissue .
Usually occur in soft tissue and in organs with collateral circulation ( lungs, brain
and intestine).
White infarction: No hemorrhage so the infracted tissue or organ appear palewhite color. Usually occur in solids organs like liver, heart, and muscles.
Hyperaemia/congestion
Disturbances of circulation is the mechanism of distribution and return of blood
to and from tissues in a manner of circular movement.
The most important disturbances in this
mechanism generally are: hyperaemia (Passive and active), congestion, edema,
shock, thrombosis, embolism and infarction.
Hyperaemia
Active engorgement of vascular beds due to
increased arteriolar inflow . Affected tissue is red (oxygenatedblood) and warm,
as arterioles and capillaries are filled with blood…
Effect of Active hyperaemia
A. It brings additional oxygen and nutrients to the affected part.
B. It helps in removal of waste materials and dilution of harmful
chemical substances by bringing more fluid.
C. It brings an additional amount of
antibodies and leucocytes to the area.
Types of hyperaemia:
1. Physiologic Hyperemia
High blood flow to the stomach and intestines during digestion
High blood flow in the muscles during exercise
2. Pathologic Hyperemia
UsuallyPost—inflammation n hyperaemia. Arteriolar dilation is a response to
inflammatory stimuli / mediators. Hyperaemia with Red coloration is a early
cardinal sign of inflammation
Gross appearance: The arteries are dilated and encourage with blood. The
affected part is swollen, enlarged and haevier than normal - If the organ is incised,
blood flows freely from the cut surface.
Microscopical appearance: The capillaries are dilated and filled with red blood
cells.
Passive hyperaemia/Venous Congestion:
Passive engorgement of a vascular bed generally caused by a decreased
outflow of blood or increase amount of blood in the venous side of the circulation,
caused by failure of drainage mechanism of the hart (Right and left), or localizes
venous obstruction.
Two types :
1. Generalized (Acute and chronic heart failure )
2. Localized (Acute and Chronic venous
obstruction)
Acute generalized passive hyperaemia (congestive heart failure):
Gross appearance; Organs (Liver , lung, mesentery) are contains much
blood and cyanotic (have a bluish-red colour) due to accumulation of nonoxygenated blood. The veins are distended with blood (the vena cava and large
veins of the abdominal and thoracic cavities) .
Microscopical appearance: The capillaries and veins are dilated and full of
blood - In the liver, the sinsusoids and in the spleen the blood spaces are filled
with blood.
Effect: When the cardiac and pulmonary changes are severe and can not be
corrected, the lack of oxygen and nutrients and the accumulation of waste
materials result in death of the cells
Chronic generalized passive hyperaemia:
Gross Appearance: Gross appearance: The veins
throughout the body are engorged with blood with Oedema of the tissue (A
transudate is found in the body cavities), atrophy of the parenchymatous organs,
and hyperplasia of connective tissue and fibrosis (in the liver called cardiac
Hepatic cirrhosis).
Microscopical appearance: The venous capillaries appear dilated and engorged
with blood, Oedema first appears perivascular - Degenerative changes in
parenchymatous organs, Other changes are:
Lung (brown induration of the lung) : There is, moreover, the picture of excessive
destruction of erythrocytes, and haemosidrin precipitates - Presence of many
macrophages engulfing golden-brown haemosidrin pigment and then called "heart
failure cells" - Fibrosis of the interalveolar septa. Induration, brown colour,
thickened alveolar septa, small hemorrhages, heart failure cells
Liver (nut meg liver): Dilatation and engorgement of the central veins of the
hepatic lobules with blood and they appear dark - Proliferation of connective
tissue around the central veins – Pericentral(peripheral) degenerative changes
including fatty change. Degenerative and necrosis due to hypoxia
Spleen (congestive spleenomegaly): The organ is enlarged and swollen due to
congestion, oedema and fibrosis
Localized passive hyperaemia :
Accumulation of blood due to obstruction of the venous drainage
in any part of the body.
Causes: 1. Iatrogenic ( pressure by bandage, tumour, lymph node , pregnancy)
2. Interstinl obstruction, torsion, strangulation
3. Venous thrombosis
Acute localized passive hyperaemia
Gross appearance: The affected tissue or organ is swollen and increased in
weight - When the organ is incised, blood oozes from the cut surface - The veins
in the area are distended, and the affecetd tissue is bluish in colour.
Microscopical appearance: Veins and capillaries are distended with blood There is oedema of the interstitial connective tissue - Disturbances of cell
metabolism or necrosis are present when loss of nutritional requirement.
Chronic local passive hyperaemia :
Gross appearance: Oedema of the organ or tissue due to increased permeability
of the capillaries as a result of hypoxia - Multiple haemorrhages are present which
are related to injury of the wall of the blood vessels - Increased connective tissue
formation and shrinkage of the organ - In chronic local passive hyperaemia, due to
gradual onset of obstruction, collateral circulation has had time to develop, and its
veins are frequently enlarged leading to the formation of "varicose veins".
Microscopical appearance: Dilatation of the obstructed veins is still
prominent - New collateral branches are seen - Degeneration and necrosis of
the cells of the organ - Increased fibrous connective tissue.
Hemorrhage
Hemorrhage generally indicates extravasation of blood . Hemorrhage may be
manifested in a variety of patterns, depending on the size, extent, and location of
bleeding.
• Hemorrhage may be external or may be enclosed within a tissue; accumulation
of blood within tissue is referred to as a hematoma.
• Minute 1- to 2-mm hemorrhages into skin, mucous membranes, or serosal
surfaces are denoted as petechiae ) and are typically associated with locally
increased intravascular pressure, low platelet counts (thrombocytopenia),
defective platelet function (as in uremia), or clotting factor deficits.
• Slightly larger (≥3 mm) hemorrhages are called purpura. These may be
associated with many of the same disorders that cause petechiae and may also
occur secondary to trauma, vascular inflammation (vasculitis),
• Larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) are called
ecchymoses and are characteristically seen after trauma. The erythrocytes in these
local hemorrhages are degraded and phagocytosed by macrophages; the
hemoglobin (red-blue color) is then enzymatically converted into bilirubin (bluegreen color) and eventually into hemosiderin (gold-brown color), accounting for
the characteristic color changes in a hematoma.
• Large accumulations of blood in one or another of the body cavities are called
hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis (in joints).
Patients with extensive hemorrhage occasionally develop jaundice from the
massive breakdown of red cells and systemic release of bilirubin.
.