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Animal Disease 1 > Vascular Disorders > Flashcards

Vascular Disorders Flashcards

1
Q

Define oedema and name the 2 types.

A

Fluid loss form circulation.

Inflammatory oedema
Non-inflammatory oedema/haemodynamic

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2
Q

Describe inflammatory oedema.

A

Exudate. Has high protein content, specifically neutrophils and may be red blood cells, which have entered the exudate due to migration.

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3
Q

Describe non-inflammatory oedema/haemodynamic.

A

Transudate. Low protein and does not contain cells.

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4
Q

What factors retain fluid in the circulation?

A

Plasma – osmotic pressure due to ions and proteins

Endothelium – selective permeability

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5
Q

What factors retain fluid in the interstitium and body cavities?

A

Interstitium low hydrostatic pressure

Interstitium osmotic pressure

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6
Q

How does an imbalance between the fluid retaining factors cause oedema?

A
  • Decreased plasma osmotic pressure
  • Increased capillary permeability
  • Increased hydrostatic pressure
  • Increased pressure of interstitium by salt retention
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7
Q

What type of blockages can cause oedema?

A

Blockage of lymphatic flow back to the heart. Either by physical/traumatic damage, chronic scarring, anything affecting lymph nodes or a tumour.

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8
Q

What are 2 causes of increased capillary hydrostatic pressure?

A

Increased venous pressure, such as in heart disease

Decreases venous outflow

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9
Q

What is the appearance of subcutaneous oedema?

A

Leaves indented mark in skin as a sign. Can happen after heart failure and surgery.

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10
Q

What is hyperaemia?

A
  • Active process where the precapillary sphincters open up
  • Allows blood to infuse widely through the capillary bed
  • Causing erythema/redness of the area
  • Cardinal signs of acute inflammation: heat, redness and then ultimately swelling
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11
Q

What is congestion?

A
  • Venous outflow from the capillary bed of stagnation
  • Passive engorgement of the vascular bed as opposed to the active process in hyperaemia
  • Conditions of hypoxia and cyanosis because of the blood that stagnating is low in oxygen
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12
Q

Describe the process of localised venous congestion.

A
  1. Compression of vessels occludes veins
  2. Blood still enters tissue via arteries
  3. Venous blood accumulates in capillaries and veins
  4. Hypoxic necrosis of tissue
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13
Q

Describe the process of generalised venous congestion.

A

Main cause is congestive heart failure.

  1. Obstruction of blood flow by decreased heart function
  2. Blood pools behind the obstruction
  3. If the problem is in the left side of the heart, there is congestion of the pulmonary circulation
  4. If the problem is in the right side of the heart, there is congestion of the hepatic circulation
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14
Q

Describe the chronic haemosiderophages in alveoli.

A
  1. Air paces and reddening of interalveolar walls.
  2. Macrophages in the alveolar spaces take up blood which is often forced out into the alveolar spaces as there is damage to the very fine capillaries due to the increasing pressure.
  3. Macrophages break down the blood and become pigmented with haemosiderin (brown cells)
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15
Q

Describe how the liver gets chronic nutmeg appearance.

A

‘Nutmeg’ appearance and congestion around central veins. Because of venous outflow, central venules start to dilate and so the parenchyma around each small vessel becomes hypoxic. Blood may still be able to enter by hepatic artery and arterioles but there is decreased venous outflow leading to chronic nutmeg appearance.

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16
Q

Describe haemoperitoneum hemorrhages.

A

Bleeding into body cavities: can see a large amount of blood clotting on top of the abdominal organs as a result of haemorrhage into the abdominal cavity.

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17
Q

Describe pulmonary haemorrhages.

A

Haemorrhage from the body, such as in eh respiratory tract, may be apparent as a nose bleeds/epistaxis or blood from the mouth. If originating from the lungs, may be whipped up into a frothy red fluid.

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18
Q

Describe haemorrhage in the GI tract or urinary tract.

A

May be the result of inflammation or ulcers in the stomach. In the stomach, it may appear as vomiting blood but haemorrhaging into the stomach may become partially digested and become very black, as thick clots or more particulate. Further down the GI tract, blood tends to stay more red, for example, dysentery. If in the UT, urine may become clouded with blood.

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19
Q

Describe insidious haemorrhage.

A
  • Trauma or damage to blood vessels due to ulceration
  • Inflammatory response
  • Insidious causes, such as damage to endothelium via a toxin, immune response, hypoxic event or coagulopathy. This is where something disrupts the normal clotting of blood – haemophilia, anticoagulants, consumption coagulopathies.
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20
Q

What is DIC?

A

Disseminating intravascular coagulation as a result of consumption coagulopathy.

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21
Q

What are petechiae and ecchymoses?

A

Petechiae are pin point haemorrhages, maybe 1-2mm in diameter.

Ecchymoses are slightly larger haemorrhages at 1-3cm in diameter.

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22
Q

What is haemostasis?

A

Cessation of blood loss after disruption of vessel wall. This is meant to be a protective mechanism and involves platelets and fibrin clots.

Platelets become activated when they are involved in blood clotting. Inactive platelet form is the quiescent form.

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23
Q

Briefly outline the clotting cascade.

A

Prothrombin > activated to thrombin > fibrinogen > fibrin

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24
Q

Describe the activity of endothelial cells before and after injury.

A

Endothelial cells, which are extremely active and very important, are normally anti-platelet and, anti-coagulant and fibrinolytic. So would normally stop clots occurring in the normal circulation. After injury, they develop a pro-coagulant function.

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25
Q

Describe pro-coagulant activities of endothelial cells.

A
  • Favour clotting
  • Platelet adhesion
  • Extrinsic clotting cascade
26
Q

Describe anti-coagulant activities of endothelial cell.

A
  • Inhibit clotting
  • Inactivation/lysis of various clotting factors
  • Inhibit platelet aggregation
  • Fibrinolytic cascade
27
Q

Why is clotting restricted and how?

A

To avoid coagulation of the entire vascular tree.

  • Antithrombin or thrombin modifiers on endothelial cells which modify or inactivate/inhibit thrombin.
  • Also indirectly activate other factors: thrombomodulin is produced by endothelial cells reduces blood coagulation by converting thrombin to an anti-coagulant enzyme instead of pro-coagulant.
  • Plasmin acts on dissolved fibrillin blood clots to leave them and to break them down. This tends to be restricted to the site of clotting by plasminogen activator inhibitors, which restrict plasminogen activity.
28
Q

Name and describe 5 coagulopathies/decreased clotting disorders.

A
  • Haemophilia – absence/defects of clotting factors
  • Liver damage leading to decreased clotting factors
  • Deficiency in vitamin K (common in herbivores that graze on a lot of sweet clover)
  • Thrombocytopaenia causing a decreased number of platelets. Bone marrow disorders and certain drugs may cause this.
  • Septicaemia and toxaemia, which cause damage to vascular endothelium. Streptokinase enzyme that can bind with plasmin and form a complex that increases its fibrinolytic and catalytic activity and reduces clotting factor 5, reducing clotting.
29
Q

When does thrombosis occur?

A

Coagulation that is inappropriate at an uninjured vessel or exaggerated coagulation of blood in a living animal. Relating this to Virchow’s triad:

  1. Change of inner surface of vessel (endothelial injury)
  2. Change of normal pattern of blood flow
  3. Change in constituents of blood (hypercoagulability)
30
Q

What might cause hypercoagulability?

A
  • Increased number of platelets
  • Increased fibrin and clotting factors
  • Decreased activity of fibrinolysis
31
Q

Name 3 examples of hypercoagubility.

A
  • Increased platelet activity from renal disease or malignancies
  • Increased clotting factor activation from renal disease, DIC or tumours
  • Metabolic abnormalities from hyperadrenocorticism
32
Q

Describe arterial/cardiac thrombi.

A
  • Usually non-occlusive
  • Sites of endothelial injury or turbulence
  • Grey-red, laminated (platelets, fibrin, RBCs)
  • Major sites: left ventricle, faulty heart valves
33
Q

Describe venous thrombi.

A
  • Occlusive
  • Sites of stasis
  • Long red-blue cast of lumen (fibrin, enmeshed RBCs)
  • Major sites: veins of distal limbs
34
Q

What are the 4 possible fates of a thrombus?

A
  • Dissolution by fibrinolysis
  • Vessel obstruction in fibrosis
  • Organisation and recanalization
  • Embolisation – fragment breaks away and lodges somewhere else
35
Q

Define an embolus.

A

Any intravascular bolus, carried form the site of origin until it lodges at a distant site. Causing partial or complete vascular occlusion and local ischaemia to the tissues supplied by that vessel.

36
Q

What are the 7 types of embolus?

A

Thromboembolism from thrombi
Fat
Fibrocartilaginous
Tumour cells
Parasites
Bacterial/infectious/septic
Gas/air

37
Q

Describe thromboembolisms.

A
  • If venous emboli, it will typically lodge in the pulmonary circulation.
  • Arterial emboli typically lodge downstream, often at bifurcation sites. For example, a saddle thromboembolus:
38
Q

Describe fat emboli.

A
  • Typically occur when bones are broken and fragments of fat from the medullary cavity
  • Can get into the circulation and travel as an embolus
39
Q

Describe fibrocartilagenous tissue thrombi.

A
  • Uncommon
  • Intervertebral disc in a dog ruptures, which can bulge into the vertebral canal
  • Material from that can get into the vessels in the vertebral canal and can travel to the lungs
40
Q

Describe malignant tumour emboli.

A

Raft of tumour cells being carried to a secondary site in metastasis

41
Q

Describe parasitic and bacterial emboli.

A

Parasitic embolus: infrequent. Heartworm larvae

Bacterial emboli: bacterial colonies lodge in capillaries and may cause an immune response at that site

42
Q

What are 3 other forms of embolus?

A
  • Foreign material may cause a secondary chronic inflammation
  • Air embolism – accidental
  • Gas emboli – such as nitrogen
43
Q

What does the outcome of an embolism depend on?

A

The extent of occlusion – presence of collateral circulation, shape of embolus, duration of vessel occlusion

Nature of embolus

Site of embolus – tissue vulnerability and if the embolus moves. Vulnerabilities include the brain, heart, and kidney are irreversibly affected by short periods of anoxia, whereas bone is relatively resistant. Where on the artery, for example, an end artery in the kidney cortex will cause a focal area of ischaemic necrosis/infarction.

44
Q

What are the common causes of ischaemia?

A

Thrombosis
Embolism
Compression
Vasoconstriction
Vasculitis

45
Q

Define infarction.

A

Death of tissue as a result of ischaemia.

46
Q

Describe the effects of infarction.

A

The effects of a short span of hypoxia or anoxia due to ischaemia may be reversible. How serious the effects of ischaemia are related to the metabolic demands of the tissue, the local circulation of the tissue, whether it is an end artery or collateral circulation, the duration of ischaemia.

47
Q

How does infarction affect different tissues?

A

Most vulnerable are the brain, kidney and heart and least vulnerable are the bones, lungs, liver and muscle, those with an alternate blood supply.

48
Q

How does artery size affect infarction?

A

Small or terminal artery = focal infarction

Large or more proximal artery = global infarction

49
Q

Define shock.

A

A state of generalised tissue hypoperfusion over a large area and possibly the whole body. Rapidly progressive and fatal.

50
Q

What is shock caused by?

A

Decreased effective circulating blood volume

And/or a decrease in the peripheral vascular resistance

51
Q

How does hypoperfusion cause shock?

A
  1. Hypoxia
  2. Shift to anaerobic metabolism
  3. Cellular degeneration
  4. Cell death
52
Q

What are 3 types of shock?

A

Hypovolaemic
Cardiogenic
Blood maldistribution

53
Q

Describe hypovolaemic shock.

A
  • Significant blood or fluid loss, perhaps sue to haemorrhage, vomiting and diarrhoea, or severe burns.
  • Reducing circulating volume
  • At a 10% decrease in blood volume, there is no fall in blood pressure as this is highly regulated.
  • At a 25% loss of volume, blood pressure decreases significantly and tissue perfusion is inadequate
54
Q

Describe cardiogenic shock.

A
  • Due to cardiac dysfunction
  • There are compensatory mechanisms largely due to the sympathetic nervous system
  • But if unsuccessful, there is stagnation of blood
55
Q

Describe blood maldistribution shock.

A
  • Increased peripheral vascular diameter
  • There is blood pooling and stagnation
  • So effective circulating volume is reduced
  • Happens in anaphylactic shock, neurogenic shock and septic shock
56
Q

How is disseminating intravascular coagulation shock exacerbated by coagulopathy?

A
  1. Widespread sepsis, damage to the endothelium or tissue destruction causes tissue factor release from the endothelial cells and platelets will be aggregated.
  2. Widespread thrombosis.
  3. Widespread vascular occlusion.
  4. Widespread ischaemia
  5. Widespread thrombi stimulate the activation of fibrinolysis and inhibit of thrombin, platelet aggregation and fibrin formation.
  6. Causes thrombi all over the body to break down.
  7. Clotting factors have been used and now there is little ability left in the blood to clot further.
  8. Because there has been ischaemic damage to the endothelium all over the body, there is widespread insidious, small haemorrhages.

In an animal that has died this way, it is apparent by hairless areas of skin and haemorrhages all over the skin in subcutaneous tissues and in most organs.

57
Q

In the general pathology of the blood circulatory system, name the process that lead to an accumulation of protein and red blood cells which forms on the endothelial lining of a vessel or the heart.

A

The process by which an accumulation of protein (fibrin), platelets and red-blood cells forms within the circulatory system and attaches itself to the endothelial lining is thrombosis. The clot itself is called a thrombus.

58
Q

Fragments of such vegetations can break off when the heart valves flap and these fragments will enter the lumen of the heart and from there exit into the bloodstream and travel elsewhere. What is the name of this process?

A

The process is embolism and the fragments themselves would be called emboli (singular: embolus). Any accumulated ‘material’ – thrombus (as in this case) – with or without infectious agents; foreign material; tumour cells; air or gas bubbles can potentially become free-floating and travel into the blood stream.

59
Q

What would be expected from the presence of bacteria in small vessels of the glomeruli?

A

The bacteria will incite an acute inflammatory response, so neutrophils will move into the vessels and surrounding area. The vessels will become plugged with fibrin, platelets and red blood cells (thrombosis), as a result of the stasis and / or turbulence in the vessels and the effects that the inflammatory response will have on the endothelial cells.

60
Q

What is to be expected from bacteria plugging the efferent arterioles of the kidney?

A

The efferent vessels to the glomerulus supply the rest of each nephron. The plugging of the vessels will cause ischaemic necrosis of the areas supplied by the small plugged vessels. An area of ischaemic necrosis in a tissue is said to be infarcted (or it is an infarct). The ischaemic cells in the infarcted area will incite an acute inflammatory response.

Animal Disease 1 (25 decks)

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