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BVSc2 AD1 > Blood problems > Flashcards

Blood problems Flashcards

1
Q

What are the two causes of engorgement of the vascular bed?

A

active - erythema

passive - congestion

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2
Q

What is active hyperaemia?

A

Engorgement of the vascular bed due to inflow of blood

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3
Q

What is passive congestion?

A

Engorgement of the vascular bed due to

decreased outflow of blood - blockage

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4
Q

What are the two types of congestion?

A

localised and generalised venous congestion

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5
Q

What causes localised venous congestion?

A

Compression of vessels occludes veins

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6
Q

What causes generalised venous congestion?

A

Obstruction of blood flow by decreased heart function

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7
Q

What does right sides congestion cause?

A

Congestion of heptic circulation

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8
Q

What does left side congestion cause?

A

Congestion of pulmonary circulation

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9
Q

What is the type of congestion seen in dead animals?

A

Hypostatic congestion

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10
Q

What is hypostatic congestion?

A

Gravity dependent reddening and blanching of pressure points

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11
Q

What is ischaemia?

A

Injury of a tissue as a result of failure in perfusion

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12
Q

What is infarction?

A

iscaemia that leads to necrosis

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13
Q

What are the two different types of infarction?

A

Focal - small artery, local infarction

Global - large artery causing extensive infarction

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14
Q

What happens during reperfusion injury?

A

when ischaemia happens mitochondria are damaged
antioxidants are used up
when O2 returns free radicals arent removed
these metabolites then go on to damage heart

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15
Q

What is oedema?

A

It is an abnormal distribution of fluid between the plasma and the interstitium that results in more fluid in the tissues or body cavities

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16
Q

What causes oedema?

A

Decreased plasma osmotic pressure
Increased capillary permeability
Increased capillary hydrostatic pressure
Decreased lymphatic drainage

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17
Q

What causes decreased plasma osmotic pressure?

A

Loss/decreased synthesis of plasma proteins

18
Q

What causes increased capillary permeability?

A

Endothelial damage from chemicals/toxins

Inflammation

19
Q

What causes increased capillary hydrostatic pressure

A

Increased venous pressure

Decreased venous outflow

20
Q

What causes decreased lymphatic drainage?

A

Lymphatic vessel compression due to neoplasia, inflammation

21
Q

What fluid is in inflammatory oedema?

A

Exudate

22
Q

What is exudate made up of?

A

High in proteins and high in cells

23
Q

What fluid is in non inflammatory oedema?

A

Transudate

24
Q

What is transudate made up of?

A

Low in protein and low in cells

25
Q

What fluid is a mixture of different amounts of protein and cells?

A

Modified transudate

26
Q

What happens in primary haemostasis?

A

vasoconstriction
platelets adhere
fibrinogen binds platelets into a plug

27
Q

What happens in secondary haemostasis?

A

Coagulation cascade
fibrin polymerisation
secondary haemostatic plug forms

28
Q

What is the word for decreased number of platelets?

A

Thrombocytopenia

29
Q

What is the word for impaired platelet function

A

Thrombocytopathy

30
Q

What is a giant bruise called?

A

Haematoma

31
Q

What are petechiae?

A

Pin point haemorrhages

32
Q

What is virchows triad?

A

Abnormal blood flow
Hypercoagulability
Endothelial injury

33
Q

What causes hypercoagulability?

A

Increased platelets/fibrin
stress
inflammation
neoplasia

34
Q

Where do occlusive thrombi form?

A

Veins

35
Q

Where does stasis thrombi occur?

A

Veins

36
Q

What are different about arterial thrombi?

A

Lines of Zahn

37
Q

What is an embolism?

A

Intravascular bolus that is carried in blood until its lodged

38
Q

What causes shock of the CV system?

A

Decreased circulating blood volume

decreased peripheral vascular resistance

39
Q

What causes hypovolaemic shock?

A

Blood/fluid loss

40
Q

What causes cardiogenic shock?

A

Ineffective heart pumping

41
Q

What causes blood maldistribution shock?

A

Anaphylaxis/neurogenic/septic
blood pooling
Decreased peripheral vascular resistance

42
Q

What is the clinical course of shock?

A 
Impaired perfusion
hypoxia
anaerobic metabolism
cell degeneration
cell death

BVSc2 AD1 (12 decks)

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