Vascular system pathology Flashcards

(41 cards)

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
Where do venous emboli lodge?
pulmonary circulatiopn
26
What is a saddle thromboembolus?
-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
Where can fat emboli come from?
fragments of fat from medullary cavity after fracture
28
Where can fibrocartilaginous emboli come from?
-from degenerate intervertebral disc, dogs -ruptured -material get into vessels and vertebral canal and travel to lungs
29
What are malignant tumour emboli?
-rafts of tumour cells -may establish as secondary tumour-metastasis
30
What are parasitic emboli?
-infrequent -vessel with profiles of one or more parasites within -inside thrombus
31
What are bacterial emboli?
-septicemia or bacteriaemia -bacterial colonies lodge in capillaries
32
What does the outcome of the embolism depend on?
-extent of occlusion -nature of embolus -site-tissue vunerability and embolus moves -brain, heart, kidney affected by short period of anaxia
33
What does a occusion at end of artery cause?
ischaemic necrosis
34
What are common causes of ischemia?
-thrombosis -embolism -compression -vasoconstriction -vasculitis
35
What are the effects of infarction dependent on?
-sensitivity to hypoxia -local circulation -duration of ischaemia
36
What is shock?
state of generalised tissue hypoperfusion caused by decrease effective circulating blood volume and/or decreased peripheral vascular resistance
37
What is hypovolaemic shock?
-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
What is cardiogenic shock?
-Cardiac dysfunction -Infarction, area of anoxia to myocardium or serious cardiac arrythias -Compensatory mechanisms (symp NS) But, if unsuccessful--> stagnation of blood
39
What is blood maldistribution?
-Increased peripheral vascular diameter -Created blood pooling/stagnation -Anaphylaxis, neurogenic, septic
40
what is disseminated intravascular coagulation?
A coagulopathy in which clotting and anticlotting mechanisms occur at the same time
41
what are the steps in disseminated intravascular coagulation
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)