Pathology of the Cardiovascular System 4 Flashcards
-Know the structure of the vessels in the arterial and venous systems -Know the factors controlling fluid balance -Explain the following as they relate to blood vessels- torsion, rupture, aneurysms, vascular thickening, vasculitis, thrombosis, and give examples using common diseases in domestic animals. -Illustrate Virchow's Triad, giving examples of disease where it is important in domestic species. -Vena caval syndrome- describe underlying processes and implications for the affected ani
THE VASCULAR SYSTEM
Consists of pulmonary and systemic circulations.
The systemic circulation carries a greater volume of blood.
Pressure decreases as we move from systemic to pulmonary (aorta to vena cavae)
Cross sectional areas increases as diameter of vessels decreases.
Velocity of flow decreases with vessel diameter.
BLOOD DISTRIBUTION WITHIN THE CIRCULATORY SYSTEM
The heart, liver, lungs and kidney have high blood flow, which is crucial as they alter/recondition blood.
At rest- 60% of blood is in the VENOUS system- it acts as a storage pool that can rapidly return blood to the heart if necessary.
Most capillaries are closed most of the time.
eg. only 10% of skeletal muscle capillaries are perfused at rest.
STRUCTURE OF THE VESSELS
Arteries, capillaries and veins.
ARTERY- Thick smooth muscle layer surrounding inner layer of endothelium, high pressure.
VEIN- Thinner smooth muscle layer, valves.
CAPILLARIES- Endothelium and basement membrane only- no smooth muscle.
Capillaries allows exchange in organs between veins and arteries (via anastomoses)
STRUCTURE AND FUNCTION OF ENDOTHELIUM
Endothelium is essential for inflammatory/oedema/haemostasis responses.
Tight junctions between cells are altered in the above responses.
Macrophages can adhere to the endothelial walls.
LYMPHATIC VESSELS
Lymphatic vessels begin in the capillary beds.
They are thin walled, blind ending vessels.
They drain tissue fluid.
HYPERAEMIA
Increased volume and pressure of blood in the capillary, causing capillary dilation, with potential for fluid extravasation.
INCREASED INFLOW causes engorgement with oxygenated blood.
Active- only seen in live animals!
Causes erythema.
CONGESTION
Increased volume and pressure of blood in the capillary, causing capillary dilation, with potential for fluid extravasation.
DECREASED OUTFLOW causes engorgement with deoxygenated blood.
Passive- can occur post mortem.
Causes hypoxia/cyanosis (blue)
FLUID PRESSURES IN VESSELS
ONCOTIC PRESSURE (colloid osmotic pressure)- proteins in vessels pull fluid in to lumen. Albumin exerts 80% of colloid osmotic pressure. Maintained by the difference in solute concentration between vessel lumen and interstitium.
HYDROSTATIC PRESSURE- pressure of fluid on the vessel walls pushes fluid OUT of vessel lumen to interstitium.
There is a delicate balance between the two. In the normal body, there is very little net loss of fluid from the vessels to the interstitium.
OEDEMA
Excessive interstitial fluid.
Forms via various mechanisms:
1. INCREASED VASCULAR PERMEABILITY- inflammatory or immunological stimulation- mediators include histamine, bradykinins, leukotrienes. Endothelial cells contract then retract.
- INCREASED INTRAVASCULAR HYDROSTATIC PRESSURE- more fluid is pushed out of vessels.
- DECREASED INTRAVASCULAR ONCOTIC PRESSURE- less fluid is pulled in to vessel lumen/protein loss changes protein gradient from vessel to interstitium, allowing protein to leave the vessel. eg. hypoalbuminaemia.
- DECREASED LYMPHATIC DRAINAGE- normally, lymphatic cells overlap. Decreased drainage means more fluid in the vessels, decreasing overlap. Fluid can leak out of the spaces between cells, causing interstitial oedema.
Lesions depend on the number and location of vessels affected.
Transudate, modified transudate, or exudate can be produced- depends on fluid composition.
INCREASED HYDROSTATIC PRESSURE
eg. Increased blood pressure, decreased venous return.
Fluid is pushed out of vessels -> oedema.
DECREASED COLLOID OSMOTIC PRESSURE
Driven by protein loss.
Fluid leaves vessels instead of being drawn in by proteins -> oedema.
CAUSES OF PROTEIN LOSS
Protein loss results in decreased oncotic pressure.
Essentially refers to albumin loss (hypoalbuminaemia), as albumin exerts 80% of colloid osmotic pressure.
1. LIVER FAILURE eg. cirrhosis. Protein production decreases.
2. INTESTINAL MALABSORPTION eg. Johne’s, IBD. Protein loss increases.
3. RENAL FAILURE eg. nephrotic syndrome. Protein is not reabsorbed.
4. PARASITIC INFECTION with severe adominal blood loss.
-> decreased oncotic pressure -> oedema
DISRUPTION OF NORMAL CIRCULATION
Torsion Rupture Vascular thickening Vasculitis Thrombosis
TORSION
Twisting of vessels.
Veins are occluded first due to their thinner walls. This leads to congestion.
If torsion continues, arteries become occluded.
This leads to necrosis, due to anoxia/ischaemia.
eg. Lipoma strangulation colic.
eg. Splenic torsion in GDV in German Shepherds- the spleen can twist die to the long gastrosplenic ligament.
RUPTURE
-Arterial rupture- commonly traumatic. Uncommonly spontaneous (racehorses- aortic rupture leads to cardiac tamponade if rupture is within pericardial sac -> sudden death. May be underlying degeneration)
-Aneurysm- LOCALISED ABNORMAL DILATION OF VESSEL.
Congenital or acquired. Infrequent except in turkeys.
Aneurysms are likely to rupture, with fatal consequences.
GUTTURAL POUCH MYCOSIS
The internal carotid artery passes over the surface of the guttural pouch.
Mycosis of the guttural pouch produces fungal plaques, which can cause rupture of the internal carotid/maxillary artery.
This presents clinically as severe epistaxis.
VASCULAR THICKENING
ARTERIORSCLEROSIS
ATHEROSCLEROSIS
Once one form of vascular thickening has occurred, the other becomes more likely.
ARTERIOSCLEROSIS
“Hardening” of the arteries.
Occurs due to old age and high blood pressure.
-Medial smooth muscle proliferation
-Fibrosis of the intima
-Narrowing of vessel lumen
-Loss of elasticity
-MINERALISATION can occur:
-DYSTROPHIC CALCIFICATION- secondary to tissue damage
-METASTATIC CALCIFICATION- due to hypercalcaemia eg. renal secondary hyperparathyroidism, paraneoplastic syndrome, vitamin D toxicity.
Johne’s disease- multiple prominent mineralised foci can be seen on the aorta. Unknown as to why these occur.
ATHEROSCLEROSIS
ACCUMULATION rather than hardening.
eg. hypothyroid dogs- lipid metabolism is depressed, leading to accumulation of plasma lipids.
Fibro-fatty plaques are deposited in vessels- consisting of lipid, fibrous tissue and calcium.
Cholesterol clefts can often be seen histologically.
Damage to endothelium leads to thrombosis (Virchow’s triad)
VIRCHOW’S TRIAD
The three broad categories that are thought to contribute to thrombosis:
- HYPERCOAGULABILITY
- STASIS OF BLOOD FLOW
- ENDOTHELIAL DAMAGE.
VASCULITIS
Inflammation of blood vessels.
Infectious (viral, bacterial, mycotic, parasitic)
Non infectious (immune mediated, toxic)
Often affects MULTIPLE organs.
Possible lesions- OEDEMA, HAEMORRHAGE, NECROSIS/INFARCTION
TRUE VASCULITIS
Inflammatory cells are present WITHIN the blood vessel wall.
This leads to degeneration of the vessel wall.
ARTERITIS
Vasculitis of arteries.
PHLEBITIS
Vasculitis of veins.
eg. Omphalophlebitis (navel ill)- the umbilical vein is infected via the urachus, becoming inflamed. Infection can track to the liver via the umbilical vein, causing hepatic abscesses.
