Pathology of the Cardiovascular System 4

Question 1

THE VASCULAR SYSTEM

Answer 1

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.

Question 2

BLOOD DISTRIBUTION WITHIN THE CIRCULATORY SYSTEM

Answer 2

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.

Question 3

STRUCTURE OF THE VESSELS

Answer 3

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)

Question 4

STRUCTURE AND FUNCTION OF ENDOTHELIUM

Answer 4

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.

Question 5

LYMPHATIC VESSELS

Answer 5

Lymphatic vessels begin in the capillary beds.
They are thin walled, blind ending vessels.
They drain tissue fluid.

Question 6

HYPERAEMIA

Answer 6

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.

Question 7

CONGESTION

Answer 7

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)

Question 8

FLUID PRESSURES IN VESSELS

Answer 8

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.

Question 9

OEDEMA

Answer 9

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.

2. INCREASED INTRAVASCULAR HYDROSTATIC PRESSURE- more fluid is pushed out of vessels.
3. 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.
4. 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.

Question 10

INCREASED HYDROSTATIC PRESSURE

Answer 10

eg. Increased blood pressure, decreased venous return.

Fluid is pushed out of vessels -> oedema.

Question 11

DECREASED COLLOID OSMOTIC PRESSURE

Answer 11

Driven by protein loss.

Fluid leaves vessels instead of being drawn in by proteins -> oedema.

Question 12

CAUSES OF PROTEIN LOSS

Answer 12

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

Question 13

DISRUPTION OF NORMAL CIRCULATION

Answer 13

Torsion 
Rupture
Vascular thickening
Vasculitis
Thrombosis

Question 14

TORSION

Answer 14

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.

Question 15

RUPTURE

Answer 15

-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.

Question 16

GUTTURAL POUCH MYCOSIS

Answer 16

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.

Question 17

VASCULAR THICKENING

Answer 17

ARTERIORSCLEROSIS
ATHEROSCLEROSIS
Once one form of vascular thickening has occurred, the other becomes more likely.

Question 18

ARTERIOSCLEROSIS

Answer 18

“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.

Question 19

ATHEROSCLEROSIS

Answer 19

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)

Question 20

VIRCHOW’S TRIAD

Answer 20

The three broad categories that are thought to contribute to thrombosis:

1. HYPERCOAGULABILITY
2. STASIS OF BLOOD FLOW
3. ENDOTHELIAL DAMAGE.

Question 21

VASCULITIS

Answer 21

Inflammation of blood vessels.
Infectious (viral, bacterial, mycotic, parasitic)
Non infectious (immune mediated, toxic)
Often affects MULTIPLE organs.
Possible lesions- OEDEMA, HAEMORRHAGE, NECROSIS/INFARCTION

Question 22

TRUE VASCULITIS

Answer 22

Inflammatory cells are present WITHIN the blood vessel wall.
This leads to degeneration of the vessel wall.

Question 23

ARTERITIS

Answer 23

Vasculitis of arteries.

Question 24

PHLEBITIS

Answer 24

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.

Question 25

PARASITIC VASCULITIS

Answer 25

Angiostrongylus vasorum (heartworm) is an
emerging pathogen in the UK.
Parasite eggs cause vasculitis as they move through capillaries in to the lungs (eggs and larvae can be seen histologically in lung tissue).
The lungs can have a yellow-green colour, due to eosinophil infiltration.

Question 26

THROMBOSIS AND OCCLUSION

Answer 26

Virchow's Triad- Hypercoagulability, stasis of blood flow, endothelial injury. 
A thrombus is a clot produced in life. 
eg. ARTERIAL- Saddle thrombi in cats
-Pulmonary artery thrombosis in dogs
-Mesenteric arteritis in horses
VENOUS- Iatrogenic
-Portal vein thrombosis
-Vena caval syndrome

Question 27

SADDLE THROMBI IN CATS

Answer 27

aka. Feline aortic thromboembolism.
Associated with hypertrophic cardiomyopathy.
Thrombus is seen at bifurcation of aorta to iliac arteries.
Secondary to LEFT ATRIAL thrombosis in 10-20% of cats with hypertrophic cardiomyopathy.
Clinical signs- pain, posterior paresis.

Question 28

MESENTERIC ARTERITIS

Answer 28

Seen in horses- inflammation and thrombosis of mesenteric arteries due to migrating strongyles.

Question 29

IATROGENIC VENOUS THROMBOSIS AND OCCLUSION

Answer 29

Seen due to long term catheterisation.

eg. Jugular vein thrombosis in the horse following catheterisation.
eg. Portal vein thrombosis. Portal vein is occluded/thrombosed, so smaller vessels must dilate and form ACCESSORY PORTAL CIRCULATION to allow blood to travel back to the heart.

Question 30

VENA CAVAL SYNDROME

Answer 30

Occlusion of the vena cava by infiltration, thrombosis or compression.
Seen in dogs secondary to heartworm infection (adult worms block vena cava) and neoplasia (eg. heart base tumour). Venous congestion and neoplasia are seen.
Seen in cattle secondary to hepatic abscesses. Hepatic venous congestion and pulmonary thromboembolism.

Question 31

HEPATIC ABSCESSES IN CATTLE

Answer 31

Abscesses in the liver erode the wall of adjacent vessels.
-> Seeding of the vascular supply
-> Abscesses can develop in other organs
-> Can lead to thrombus formation and lodging in the caudal vena cava
-> Embolic arteritis and aneurysm
-> Haemoptysis (coughing/spitting much foamy blood due to bleeding in respiratory tract)
CAN BE FATAL.

Question 32

LYMPHATIC DISEASES

Answer 32

Lymph vessels are thinner walled than blood vessels, but show a similar range of lesions.

• LYMPHANGIECTASIS- dilation of lymph ducts eg. intestinal lymphangiectasia.
• RUPTURE OF LYMPHATIC DUCTS
• LYMPHANGITIS- inflammation of lymph ducts.

It is normal for lymphatic ducts to be very prominent following a large meal!
The cisterna chyli is located at the caudal end of the thoracic duct.

Question 33

RUPTURE OF LYMPHATIC DUCTS

Answer 33

CHEST- Thoracic duct rupture

• > Chylothorax (lymph fluid in thoracic cavity)
  eg. due to thymic lymphoma obstructing thoracic duct.

ABDOMEN- Cisterna chyli rupture -> chylous ascitse (fluid in abdominal cavity)

Question 34

LYMPHANGITIS

Answer 34

• Systemic infections- granulomatous lymphangitis eg Johne’s disease, actinobacillosis.
• Idiopathic- sporadic lymphangitis can be seen in horses.