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PVS Pathology week > Haemodynamic disorders, thrombosis and shock > Flashcards

Haemodynamic disorders, thrombosis and shock Flashcards

1
Q

What is meant by microcirculation?

A

The exchange of fluid, nutrients and waste products between blood and cells taht takes place through the interstitium and microcirculation.

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2
Q

What is the interstitium?

A

Space between cells. Composed of structural, adhesive and absorptive components

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3
Q

Describe the fluid distribution in the body

A

Body= 80% water (2/3 intracellular. 1/3 extracellular)

extracellular= 80% in the interstitium and 20% in plasma

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4
Q

What helps control distribution of fluid nutrients and waste between blood/ interstitium and cells?

A
  • Physical barriers
  • Pressure
  • Concentration gradients
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5
Q

What is the definition of oedema?

A

Accumulation of excess interstitial fluid

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6
Q

What are the mechanisms of oedema?

A
  • Increased microvascular permeability
  • incrased intravascular hydrostatic pressure
  • decreased intravascular osmotic pressure
  • decreased lymphatic drainage
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7
Q

What are the causes of increased microvascular permeability?

A
  • Inflammation
  • Toxins
  • Anaphylaxis
  • Clotting abnormalities
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8
Q

What are the causes of increased intravascular hydrostatic pressure

A
  • Portal hypertension
  • Pulmonary hypertension
  • Localised hypertension
  • Localised venous obstruction
  • Fluid overload
  • Hyperaemia
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9
Q

What are the causes of decreased intravascular osmotic pressure?

A
  • Decreased albumin production
  • Increased albumin loss
  • Water intoxication
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10
Q

What are the causes of decreased lymphatic drainage?

A
  • Lymphatic obstruction/ compression
  • Lymphagitis
  • Lyphatic aplasia/ hypoplasia
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11
Q

What is the definition of haemostasis?

A

Arrest of bleeding.

  • The physiologic response to vascular damage, mechanism to seal an injured vessel
  • Interactions between endothelium, platelets and coagulation factors
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12
Q

What are the three stages of haemostasis?

A

1) formation of platelet plug (primary haemostasis)
2) formation of fibrin network (secondary haemostasis)
3) Removal of platelet/ fibrin plug (fibrinolysis) (thrombus retraction)

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13
Q

Explain the extrinsic coagulation pathway

A

Occurs outside the blood vessel wall when shed blood contacts tissue debris. Involves THROMBOPLASTIN.

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14
Q

Explain the intrinsic coagulation pathway

A

Triggered by presence of abnormal surfaces on components normally present in the blood (all the coagulation factors). Finishes with activation of Factor X.

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15
Q

What is the other name for Factor 3 in the coag cascade?

A

Tissue factor/ Thromboplastin

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16
Q

What is Factor VII in the coag cascade?

A

Proconvertin

17
Q

Which factor is at the terminus of the extrinsic and intrinsic pathways of the coag cascade?

A

Factor X

18
Q

What is the end product of the coag cascade?

A

Fibrin

19
Q

What is the name for too low concentration of platelets?

A

Thrombocytopenia

thrombocytopathy= name for abnormal platelet function

20
Q

What is Petechia?

A

Pinpoint haemorrhage (1-2mm)

21
Q

What is ecchymosis?

A

Haemorrhage of up to 2-3cm

22
Q

What does the thrombosis Virchow triad include?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability
Thrombosis in the centre

23
Q

What is an embolus?

A

A piece of free floating foreign material within the blood e.g. fat, cartilage, thrombus fragment

24
Q

What is a thromboembolus?

A

Embolus derived from fragments of a thrombus

25
Q

Where do venous thromboemboli typically lodge?

A

Pulmonary circulation

26
Q

Where do arterial thromboemboli normally lodge?

A

Sites of vascular bifurcation.

27
Q

What does disseminated intravascular coagulation (DIC) mean?

A

Serious manifestation of abnormal coagulation, severe dyshomeostasis caused by the generation of excess thrombin.
Various causes e.g. diffuse vascular damage or systemic infections

28
Q

What is the mechanism for DIC?

A

Excess thrombin- platelet aggregation and fibrin formation- widespread microvascular clots- consumption of coagulation factors- widespread haemorrhages

29
Q

Describe hyperaemia

A

Increased blood flow- active engorgement of vascular beds
-increased inflow via arteriolar dilation
-outflow remains normal or is decreased.
-causes: heat (skin_ postprandial (GI)
pathologic cause= inflammation

30
Q

Describe congestion

A
  • Decreased blood flow, passive engorgement of vascular beds with a decrease outflow and normal or increased inflow.
  • Causes: acute-heart failure/ euthanasia. Chronic- obstruction of venous outflow, heart failure, pulmonary disease
31
Q

What are the causes of decreased tissue perfusion?

A
  • Obstruction of a blood vessel
  • Local vascular congestion
  • Decreased cardiac output
32
Q

What factors influence development of an infarct?

A
  • nature of the vascular supply
  • rate at which occlusion develops
  • vulnerability to hypoxia (neurons/ myocardial cells vulnerable)
  • oxygen content of the blood
33
Q

What would an arterial obstruction lead to?

A

loss of blood downstream resulting in abrupt coagulative necrosis

34
Q

What would venous obstruction lead to?

A

Reduction/ loss of venous return

35
Q

List the events of shock

A

Hypotension- decreased tissue perfusion- cellular hypoxia- shift to anaerobic metabolism- cellular degeneration- cell death

36
Q

What are the different types of shock?

A

1) cardiogenic: failure of heart to pump adequately
2) hypovolaemic: decreased circulating blood volume due to blood/ fluid loss
3) blood maldistribution: Anaphylactic (generalised type 1 hypersensitivity), neurogenic (trauma to NS), septic (peripheral vasodilation caused by components of bacteria/ fungi inducing release of vascular/ inflammatory mediators)

PVS Pathology week (7 decks)

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