Vascular system pathology Flashcards

1
Q

What factors favor fluid retention in the interstitium and body cavities?

A
  • Low hydrostatic pressure
  • Osmotic pressure
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2
Q

What factors retain fluid within circulation?

A
  • Higher oncotic pressure in plasma due to ions & proteins
  • The selective permeability of the endothelium which can open to allow fluid & ions through
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3
Q

What is exudate (inflammatory) oedema classified as?

A

Serous, fibrinous and suppurative

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4
Q

How does oedema form when there is a imbalence on fluid retaining factors?

A
  • decreased plasma osmotic pressure
  • Increase in capillary permeability, hydrostatic pressure and in osmotic pressure of interstitium (salt retention)
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5
Q

How does a lymphatic blockage cause vessel damage?

A
  • vessel damage or scarring with fibrosis
  • nodule pathology (tumour, hyperplastic inflammatory response))
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6
Q

What can lead to increased caillary hydrostatic pressure in terms of blood stagnation?

A

Increased capillary hydrostatic pressure caused by increased venous pressure from heart disease or with decreasing venous outflow

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7
Q

What are the different ways oedema could present?

A
  • Ascites (fluid filling abdomen).
  • Hydrothorax
  • Subcutaneous oedema
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8
Q

What is hyperaemia?

A

increase inflow of blood causing erythema and acute inflammation

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9
Q

What is localised venous congestion?

A
  • e.g intestinal torsion
    • vessel compression occludes veins but blood still enters via arteries
    • venous blood accumulates in capillaries and veins
    • Hypoxic necrosis of tissue
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10
Q

What is generalised venous congestion?

A
  • obstruction of blood flow due to decreased heart function
  • blood retains behind obstruction
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11
Q

What tissue is affected if there is congestion on the left side of the heart?

A

pulmonary circulation congestion

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12
Q

What tissue is affected if there is congestion on the right side of the heart?

A

hepatic circulation congestion

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13
Q

What does generalised congestionin the lungs?

A
  • Diffuse reddening
  • Darkening due to the process of hypostatic congestion
  • Oedema
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14
Q

What is the appearnace of congestion in the liver?

A

In liver there is a nutmeg appearance and there is a congestion around the central veins

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15
Q

How does a haemorrhage present in the GIT or UT?

A

-inflammaiton or ulcers
-haematemesis
-melena
-dysentry

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16
Q

What is insidious haemorrhage?

A

-damage to endothelium
-coagulopathy

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17
Q

what are the types of coagulopathies?

A

-haemophilia
-anticoagulants
-consumption coagulopathies

18
Q

What is Thrombocytopenia?

A

platlet deficiency in the blood

19
Q

What is Septicaemia?

A

blood poisoning - large amount of bacteria entering blood stream

20
Q

How can clotting be restricted?

A

avoid coagulation of the entire vascular tree
-thrombomodulin converts thrombin to anticoag enzyme
-plasmin cleaves fibrin

21
Q

What are causes of hypercoagulability?

A

-increased number of platelets
-increased fibrin, clotting factors
-decreased activity of fibrinolysis

22
Q

What are thhe different fates of a thrombus?

A
  1. dissolution (fibrinolysis)
    2.vessel obstruction (fibrosis)
  2. organisation and recanilisation
  3. embolisation- fragment breaks away
23
Q

What are the different types of embolism’s?

A

-from thrombi-thromboembolism
-fat
-fibrocartilagenous
-tumour cells
-parasites
-bacterial/infectious/septic
-gas/air

24
Q

Where do arterial emboli lodge?

A

downstream at bifurcation sites

25
Q

Where do venous emboli lodge?

A

pulmonary circulatiopn

26
Q

What is a saddle thromboembolus?

A

-in distal aorta where bifurcates to form iliac arteries
-thrombi form and more or less occlude iliac artery
-signs of pain and coldness in hindfeet

27
Q

Where can fat emboli come from?

A

fragments of fat from medullary cavity after fracture

28
Q

Where can fibrocartilaginous emboli come from?

A

-from degenerate intervertebral disc, dogs
-ruptured
-material get into vessels and vertebral canal and travel to lungs

29
Q

What are malignant tumour emboli?

A

-rafts of tumour cells
-may establish as secondary tumour-metastasis

30
Q

What are parasitic emboli?

A

-infrequent
-vessel with profiles of one or more parasites within
-inside thrombus

31
Q

What are bacterial emboli?

A

-septicemia or bacteriaemia
-bacterial colonies lodge in capillaries

32
Q

What does the outcome of the embolism depend on?

A

-extent of occlusion
-nature of embolus
-site-tissue vunerability and embolus moves
-brain, heart, kidney affected by short period of anaxia

33
Q

What does a occusion at end of artery cause?

A

ischaemic necrosis

34
Q

What are common causes of ischemia?

A

-thrombosis
-embolism
-compression
-vasoconstriction
-vasculitis

35
Q

What are the effects of infarction dependent on?

A

-sensitivity to hypoxia
-local circulation
-duration of ischaemia

36
Q

What is shock?

A

state of generalised tissue hypoperfusion
caused by decrease effective circulating blood volume and/or decreased peripheral vascular resistance

37
Q

What is hypovolaemic shock?

A

-Blood/fluid loss–> reduced circulating bolume
-Haemorrhage, diarrhoea or severe bones
-10% decrease in blood vol- no fall in BP
>35% loss of vol, BP falls significatnyl, tissue perfusion inadequate

38
Q

What is cardiogenic shock?

A

-Cardiac dysfunction
-Infarction, area of anoxia to myocardium or serious cardiac arrythias
-Compensatory mechanisms (symp NS)
But, if unsuccessful–> stagnation of blood

39
Q

What is blood maldistribution?

A

-Increased peripheral vascular diameter
-Created blood pooling/stagnation
-Anaphylaxis, neurogenic, septic

40
Q

what is disseminated intravascular coagulation?

A

A coagulopathy in which clotting and anticlotting mechanisms occur at the same time

41
Q

what are the steps in disseminated intravascular coagulation

A
  1. TF release and platelet aggregation
  2. widespread thrombosis
  3. activation of fibrinolysis/inhibition of thormbin, platelet activation and fibrin formation OR widespread vascular occlusion
  4. lysis of thrombi and consumption of clotting factors OR widespread ischaemia
  5. widepread haemorrages (or widepread ischaemia)