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Hyperemia
The term ______ literally means “too much blood” and refers to the volume and flow change. There is an active engorgement of vascular beds with a normal or decreased outflow of blood resulting in an excess amount of blood in an organ.
Active hyperemia
active arteriolar engorgement of the vascular bed.
Passive hyperemia (Congestion)
too little blood being removed by the venules.
Passive hyperemia (Congestion)
too little blood being removed by the venules.
Red
What is the appearance of hyperemia?
Tissues become bright red and warm since arterioles and capillaries are filled (engorged) with blood (red blood cells).
Why does Hyperemia manifest that color?
blood flow to the stomach and intestines during digestion
blood flow in the muscles of athletes during exercise
blood flow in skin to dissipate heat
neurovascular hyperemia (blushing)
in congestion as in erectile tissues during stimulation
Examples of Physiological Hyperemia
Pathological Hyperemia
commonly known as venous congestion or simply congestion and it occurs as a manifestation of some alterations in blood flow characteristics. It is however not the cause of this alteration, but the result of some underlying pathological process (e.g. hyperemia of inflammation).
A.By physical obstruction of either small or large vessels
B. By failure of forward flow as in heart failure.
Causes of Pathological Hyperemia
poor oxygenation of venous blood
Why does dilated venules and capillaries and the tissue appears blue or dark reddish?
duration of hyperemia, extent of hyperemia, and the mechanism by which it occurred.
3 factors are considered in the classification of pathological hyperemia
Acute
abrupt on set with rapid development
Chronic
slow developing, present for a long period of time.
Based on the extent of Hyperemia (General)
throughout an organ or system. It involves central circulation of heart and major circulation of the heart and major vessels including the lung since all the blood must flow to these organs. Congestion in this case may be caused by the following factors:
based on the extent of hyperemia (Local)
confined to discrete area. An example is a strangulated piece of intestine in which the compression on the vessels is such that arterial blood still gets in through the muscular arteries but the pressure in the thinner walled veins restricts the flow and venous blood accumulates.
Based on the mechanisms involved (active)
increase in arteriolar inflow; arteriolar-mediated engorgement of vascular bed
engorgement of the vascular bed; venous obstruction (impedance).
a. Acute Local Active Hyperemia
b. Acute Local Passive Hyperemia
c. Chronic Local Passive Hyperemia
d. Chronic General Passive Hyperemia
four basic patterns of hyperemia
Acute Local Active Hyperemia
Occurs in inflammation and is due to engorgement of the vascular bed following an increase in arteriolar blood flow into an area. The increase in arteriolar flow opens new capillary beds and newly dilated small vessels extend the arteriolar blood pressure into smaller vascular channels. This is a chemically mediated response of the microvascular to histamine, bradykinins, and other vasoactive amines.
Acute Local Passive Hyperemia
Refers to passive engorgement of the drainage area due to venous drainage. As a result, the blood backs up to the microvasculature and local venous engorgement occurs
Occurs when an organ or organ system develop chronic inflammatory lesions w/c progresses to fibrosis and therefore obstruction or impediment in the tissue’s venous drainage.
Chronic general positive hyperemia
Involves either the heart or the lungs as the major site of underlying pathological change. Depending on the nature of lesion and its location in the heart, the tissues that will suffer will either be the liver or the lungs. If the lesions occur in the left side of the heart, the lungs will be affected while if the right side of the heart is affected, the liver and the intestine will suffer.
Congestive Heart Failure
If the heart is the source of problem, the generalized passive hyperemia that results is called
The cut surfaces of congested tissues are dark red to brown and wet. Blood oozes on cut section.
Wet - due to edematous tissue.
Describe the gross Appearance of Congestion:
Acute - Associated with capillaries engorged with blood usually some edema.
Chronic - Engorgement by poorly oxygenated venous blood
Histological Appearance of Congestion:
True. Because the increase in blood can result in an increase in hydrostatic pressure and endothelial damage resulting in edema. Therefore congestion, hyperemia and edema are frequently encountered together
True or False and Why?
Both Hyperemia and Congestion indicate a local increase in blood volume.
Edema
The accumulation of too much fluid in the extracellular water in the interstitial fluid spaces (outside the vascular fluid compartment and the cellular fluid compartment) including the body cavities.
Starling equilibrium
achieved by the balance of filtration pressure exerted across the filtering membrane (capillary endothelia) of the terminal vascular bed.
The net filtration pressure
Is the difference between the plasma hydrostatic pressure and the tissue hydrostatic pressure and interstitial cell colloid osmotic pressure in the arterial end of capillary vascular bed.
the net absorption pressure
is the difference between the plasma hydrostatic pressure and the tissue hydrostatic pressure at the venous end of the capillary bed. Disturbances resulting to alteration in the balance of the forces opening in the vascular bed could lead to the accumulation of fluid in the interstitial spaces.
Local - may occur in most organ or tissues depending upon local causes.
Generalized - Affects the whole body but most of the fluid accumulate in the lower portion of the body.
Classification of Edema
Increased microvascular permeability
Increased intravascular hydrostatic pressure
Decreased intravascular osmotic pressure
Lymphatic obstruction
What are the four basic mechanisms of the development of edema.
increase in vascular permeability
most associated with the initial microvascular reaction to inflammatory or immunologic stimuli. Thus, it describes as “edema of inflammation”. Various mediators of inflammation (e.g. histamine, bradykinin, leukotrienes, and substance P) are vasoactive and increase vascular permeability.
increase intravascular hydrostatic pressure
occurs in disease conditions that increase the capillary pressure by raising the venous pressure and not by arterial pressure. Thus, the increase in the venous back pressure negates the absorptive function of the venous end. This result to a condition where fluids filtered at the arterial end failed to return to the circulation.
Decreased intravascular osmotic pressure
results from decreased concentration of plasma proteins (albumin) which can occur in hypoproteinemia (or hypoalbuminemia). Loss of large part of the albumin and globulin of the blood occurs in the nephritis characterized by sever albuminuria.
Lymphatic obstruction
usually a result to local edema. This may occur in disease conditions such as obstruction of lymphatics by growing neoplasms, obstruction by emboli and damage to lymphatics following surgical intervention.
1. severity of edema
2. rapidity of onset
3. extent of edema
4. anatomic location of edema
5. underlying cause of edema
changes produced by edema are dependent on the following factors:
Acute or rapid onset
Wet, gelatinous, and heavy, where organs are swollen, has firm and doughy consistency.
Tissue pits on pressure and indentations remain after pressure is removed
Tissue is cool to touch (unless inflammation is also present)
Fluid weeps from cut surface, although there might be slight clotting (In several species [horses and some breeds of cattle], fluids are slightly yellow).
Gross Appearance of Edema
Subcutaneous edema
Different distributions, depending on the cause
Can be diffuse or may be more conspicuous at sites of highest hydrostatic pressures
In this case, distribution is frequently gravity dependent
Ascites edema
at necropsy, edema is recognized presence of clear, yellow-tinged fluid that distends loose connective tissue or accumulates in body cavities (i.e. peritoneal, pleural, pericardial)
Anascara
septicemia due to systemic bacterial infection that produce bacterial toxins that caused vascular leakage of protein resulting in total body edema
E. coli
Bacteria strain that causes edema to pig which produce toxins that acts on endothelial cells → allowing fluid to leak out
Pink
Microscopic appearance if edema fluid is protein-rich
Clear
Microscopic appearance if edema fluid id protein-poor.
Hyperemia
Blood vessels filled with erythrocytes
Parasitic, nutritional, cardiac, or renal
Edema can be caused by?
Dependent Edema
edema fluids that are collected in the lowermost portion of the body such as the ventral abdomen and the limbs.
Ascites/Hydroperitoneum
accumulation of edematous fluid in the peritoneal cavity
Anasarca
generalized subcutaneous edema (can be seen in aborted fetus)
Hydrothorax
accumulation of edematous fluid in the thoracic cavity.
Hydropericardium / Pericardial effusion
accumulation of edematous fluid in the pericardial sac.
Hydrocoele
accumulation of edematous fluid in the scrotum.
Hydrops amnii
non – inflammatory edema of the amniotic sac.
Pitting edema
a severe and generalized edema that a finger can be pushed against the edematous tissues and produce a dent.
Lymphatic blockage
result in an inability of the lymphatics to remove normal fluid excess in the interstitium resulting in edema. This may result from surgery or trauma damaging lymphatic system; neoplastic cells obstructing normal flow of lymph; parasites obstructing flow; or a hereditary malformation of the lymphatic system.
Lymphangiectasia
dilatation of lymphatic vessels.
Lymphedema
accumulation of lymph in subcutaneous tissues.
Increased microvascular permeability
Increased intravascular hydrostatic pressure
Decrease intravascular osmotic pressure
Decrease lymphatic drainage
the major mechanisms of edema and the conditions that affect them.