Pathology of the Cardiovascular System 4 Flashcards Preview

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Flashcards in Pathology of the Cardiovascular System 4 Deck (34):
1

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.

2

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.

3

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)

4

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.

5

LYMPHATIC VESSELS

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

6

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.

7

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)

8

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.

9

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.

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.

10

INCREASED HYDROSTATIC PRESSURE

eg. Increased blood pressure, decreased venous return.
Fluid is pushed out of vessels -> oedema.

11

DECREASED COLLOID OSMOTIC PRESSURE

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

12

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

13

DISRUPTION OF NORMAL CIRCULATION

Torsion
Rupture
Vascular thickening
Vasculitis
Thrombosis

14

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.

15

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.

16

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.

17

VASCULAR THICKENING

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

18

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.

19

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)

20

VIRCHOW'S TRIAD

The three broad categories that are thought to contribute to thrombosis:
1. HYPERCOAGULABILITY
2. STASIS OF BLOOD FLOW
3. ENDOTHELIAL DAMAGE.

21

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

22

TRUE VASCULITIS

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

23

ARTERITIS

Vasculitis of arteries.

24

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.

25

PARASITIC VASCULITIS

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.

26

THROMBOSIS AND OCCLUSION

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

27

SADDLE THROMBI IN CATS

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.

28

MESENTERIC ARTERITIS

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

29

IATROGENIC VENOUS THROMBOSIS AND OCCLUSION

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.

30

VENA CAVAL SYNDROME

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.

31

HEPATIC ABSCESSES IN CATTLE

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.

32

LYMPHATIC DISEASES

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.

33

RUPTURE OF LYMPHATIC DUCTS

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)

34

LYMPHANGITIS

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