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Y3 IWB > PATHOLOGY- Essentials of general pathology - Haemodynamic disorders > Flashcards

PATHOLOGY- Essentials of general pathology - Haemodynamic disorders Flashcards

1
Q

What is haemostasis

A

Process by which blood clots form at sites of blood vessel wall damage/ injury

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2
Q

What are the 2 mutually reinforcing processes in haemostasis

A

Primary and secondary haemostasis

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3
Q

List the sequence of events in haemostasis when a blood vessel is injured

A
  1. Vasoconstriction
  2. Primary haemostasis (platelet plug formation via exposure of collagen / vWF)
  3. Secondary haemostasis (fibrin meshwork formation via exposure of tissue factor)
  4. Clot stabilisation / resorption
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4
Q

What causes vasoconstriction
What is the purpose of vasoconstriction

A

Neurogenic factor secretion
This acts as a temporary fix, reducing blood flow

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5
Q

what is the purpose of primary haemostasis

A

Formation of platelet plug

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6
Q

List the steps in primary haemostasis

A
  • Endothelial disruption causes exposure of collagen & VWF on ECM
  • Platelets adhere to VWF via glycoprotein 1b
  • Activated -> change shape “spike” > ^ surface area
  • Secrete granules -> recruit more platelets
  • Aggregate to form platelet plug
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7
Q

What is the purpose of secondary haemostasis

A

Deposition of fibrin meshwork through the coagulation cascade

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8
Q

List the steps in secondary haemostasis

A
  • Tissue factor exposed (normally expressed on sub-endothelial / fibroblast cells)
  • Activates coagulation cascade via activation of factor VII - -> thrombin formation
  • Thrombin -> cleaves soluble fibrinogen -> insoluble fibrin -> fibrin meshwork
  • Thrombin -> also activates more platelets
  • RBC entrapment
  • Acts to consolidate primary haemostasis
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9
Q

What is the coagulation cascade

A

Cascade of enzymes going from inactive to active form

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10
Q

List the steps in the coagulation cascade

A
  1. Exposed tissue factor activates factor VII to factor VIIa
  2. This activates cascade
  3. Prothrombin is converted in to thrombin
  4. Thrombin
    - Converts fibrinogen (soluble) -> fibrin clot (insoluble)
    - Activates more platelets
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11
Q

What is clot stabilisation

A

Platelet aggregates & polymerised fibrin entrap RBCs to form solid clot

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12
Q

How is clotting regulated

A

Blood dilution of coagulation factors

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13
Q

What is fibrinolysis

A
  • Activated by t-PA from endothelial cells
  • Catalyses plasminogen -> plasmin
  • Fibrin is degraded by plasmin
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14
Q

What is the role of normal endothelial cells in clot stabilisation and resorption

A
  • Shield blood constituents from TF, VWF, collagen
  • Also expresses factors to inhibit coagulation cascade, platelet aggregation and promote fibrinolysis (t-PA)
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15
Q

What happens if endothelial cells in clot stabilisation and resorption become damaged

A

Lose abilities
Become pro-thrombotic

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16
Q

What is atherosclerosis

A

Chronic inflammatory / healing response to BV injury

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17
Q

How does atherosclerosis occur

A
  1. Stimulus causes endothelial damage which increases permeability
  2. Lipid (LDL) accumulation due to increase in permeability. Platelet/monocyte adhesion at site of damage
  3. Macrophage migration and activation. Platelet/macrophages -> smooth muscle recruitment
  4. Macrophage/smoot muscle lipid uptake and T cell activation
  5. Increase in smooth muscle/ECM. Atheromatous plaque formed
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18
Q

Describe what can happen after an atherosclerotic plaque is formed

A
  • plaque grows causing critical stenosis
  • vessel wall weakening, can develop an aneurysm and rupture
  • plaque can rupture exposing VW and tissue factors and including thrombosis by inappropriate activation of primary homeostasis and secondary homeostasis
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19
Q

how can atherosclerosis lead to myocardial ischaemia

A

Atherosclerotic plaque formed
Plaque ruptures activating inappropriate activation of hemosatsis mechanisms
This results in thrombus formation

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20
Q

What is thrombosis

A

The inappropriate activation of normal haemostatic mechanisms which results in the formation of a “thrombus”

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21
Q

What is a thrombus

A

Structured solid mass or plug of blood constituents formed within the heart or blood vessels during life

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22
Q

What 3 factors contribute to thrombosis
What are they known as

A

Endothelial injury (the dominant mechanism)
Abnormal blood flow
Hypercoagulability

Virchows triad

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23
Q

How does endothelial injury lead to thrombosis

A
  1. Severe injury causes exposure of TF/VWF through plaque rupture
  2. Even if vessel isn’t severely damaged, noxious stimuli (such as physical injury, infection, abnormal blood flow, inflammatory mediators, toxins) can turn normal endothelium in to abnormal endothelium through a pro thrombotic endothelial state
  3. Endothelial cell activation/dysfunction occurs. Pro-coagulant effects cause a decrease in Thrombomodulin, protein C, tissue factor protein inhibitor. Anti-fibrinolytic causes increases in plasminogen activator inhibitors which causes decrease in t-PA
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24
Q

How does abnormal blood flow load to thrombosis

A
  1. Turbulence contributes to thrombosis in the heart and arteries. Stasis generally contributes to thrombosis in veins but sometimes in the heart/arteries, E.g. myocardial infarction/ aneurysms
  2. Endothelial cell activation -> “pro-thrombotic”
  3. Disrupts normal ‘laminar’ flow -> platelets interact with / touch endothelium
  4. Prevents washout / dilution of clotting factors
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25
Q

What is hypercoagulability

A

Abnormal tendency for blood to clot, typically through alterations in coagulation factor function

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26
Q

Endothelial injury leads to what

A

Hypercoagulability
Abnormal blood flow

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27
Q

abnormal blood flow leads to what

A

Hypercoagulability
Endothelial injury

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28
Q

What is the most common cause of hypercoagulability in the inherited form (primary)

A

Factor V Leiden mutation

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29
Q

What can cause secondary hypercoagulability

A

Cancer
Prolonged bed rest
Myocardial infarction

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30
Q

What is another name for venous thrombosis

A

Phlebothrombosis

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31
Q

How does venous thrombosis usually occur

A

Through stasis as the dominant mechanism
Occurs at site of stasis
Most commonly deep veins of legs (DVT)

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32
Q

How does arterial/cardiac thrombosis occur

A
  • Endothelial injury and / or abnormal flow (turbulence) = dominant mechanisms
  • occurs at sites of endothelial injury e.g. atherosclerosis / endocarditis
  • occurs at sites of turbulent blood flow e.g. vascular bifurcation / prosthetic valve
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33
Q

After thrombosis has occurred, what things can occur next

A
  • Propagation
  • Get larger by accumulation of fibrin/platelets
  • Dissolution (via fibrinolysis)
  • Organisation & recanalization
  • Similar to granulation tissue formation
  • In-growth of endothelial cells with formation of new blood vessel channels

Embolisation

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34
Q

Define embolisation

A

Formation of a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin (little bit breaks off and goes elsewhere)

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35
Q

Define embolism

A

The impaction of an embolus in a vessel whose calibre is too small to allow the embolus to pass leading to vascular occlusion (the little bit broken too big to fit through, getting stuck)

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36
Q

Almost all emboli are what

A

Thromboemboli

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37
Q

What are thromboemboli

A

Embolus derived from part of a dislodged thrombus (the little bit that was broken off)

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38
Q

List other types of emboli (more rare than thromboemboli)

A
  • ATHEROSCLEROTIC
  • bits of atherosclerotic plaque are broken off in to bv
  • INFECTIVE
  • Vegetations infected heart valves, mycotic aneurysm
  • TUMOUR
  • Fragmentation as tumours penetrate vessels
  • GAS EMBOLISM
    Chest trauma / iatrogenic (>100 ml)
  • Rapid decompression during diving -> nitrogen
  • AMNIOTIC FLUID
  • AF into uterine veins
  • FAT EMBOLISM
    Trauma -> break of long bones, burns, soft tissue injury, CPR
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39
Q

Where do venous emboli occur

A
  • Venous system (most commonly legs), can lead to pulmonary embolism
40
Q

Where do arterial/systemic emboli occur

A
  • Arterial system - brain, limbs, organs
  • e.g. Heart (AF,MI), aneurysms etc.
41
Q

What is a paradoxical embolism

A

When you have an embolus which has arisen in the venous circulation, that travels through the inferior vena cava into the right side of the heart but instead of passing into pulmonary circulation, it goes straight through from venous to systemic circulation (if the pt has a defect in the heart, e.g. hole in heart)

42
Q

What is a pulmonary embolism

How many deaths caused per year in UK

If untreated, what % is the risk of death

A

Obstruction of pulmonary arterial vessel by an embolus (usual thromboembolus)

60000

87%

43
Q

What does the majority of pulmonary embolism result from

A

Deep vein thrombosis

44
Q

What happens if there is fragmentation of DVT

A
  • Embolus enters inferior vena cava
  • Passes through right heart
  • Impaction and occlusion in pulmonary circulation
45
Q

Blood clots that occlude the large pulmonary arteries are virtually always what in origin

A

Thromboebolic (DVT)

46
Q

How common is pulmonary artery thrombosis

A

Rare

47
Q

What are the 5 classical histories someone with a pulmonary embolism may have

A
  • 5d post hip replacement
  • Sudden onset
  • Dyspnoea (shortness of breath)
  • Hypoxia
  • Tachycardia
48
Q

What do the effects of a pulmonary embolism depend on

A

The size of the vessel blocked

49
Q

What are the effect of large pulmonary vessels being blocked

A
  • Main pulmonary artery
  • Straddle bifurcation - “saddle” embolus - death!
  • PEs beyond bifurfaction but proximal can also be fatal
  • Obstruction of 60% of pulmonary flow = death
  • True cause of instantaneous death
50
Q

What is a block in the main pulmonary artery known as

What does it cause usually

What else can be fatal

A

Straddle bifurcation causing a saddle embolus

Death (true cause of instantaneous death)

Pulmonary embolism beyond bifurcation but proximal

51
Q

Obstruction of __ of __ can cause death

A

60%

Pulmonary flow

52
Q

What are the effects of smaller vessels being occluded in pulmonary embolism

A

Dyspnoea (breathlessness)
Pleuritic chest pain (pain on inspiration)

53
Q

Why do most people not know they have smaller vessel occlusion

A

Asymptomatic (60-80% clinically silent)

54
Q

What 2 things does systemic thromboembolism cover

A

Cardiac
Arterial

55
Q

Where does systemic thromboembolism occur

A

Within the arterial circulation

56
Q

80% of systemic thromboemboli arise from what

A

Intro-cardiac mural thrombi (myocardial infarction, atrial fibrillation, etc)

57
Q

Systemic thromboembolism can arise from what else

A
  • Aortic aneursym thrombus
  • Atherosclerotic thrombus
  • “Paradoxical embolism”
58
Q

What is the result of systemic thromboembolism

A

Ischaemic injury (75% to limbs, 10% to brain, 15% to other viscera)

59
Q

What can a paradoxical embolism have an effect on

A

Brain, limbs, organs (systemic)

60
Q

Atherosclerosis, thrombosis and embolism causes damage to organs through what 2 things

A

Ischaemia and infarction

61
Q

what is ischaemia

A

Localised tissue hypoxia resulting from a reduction in blood flow to an organ or tissues

62
Q

Define hypoxia

A

A state of reduced oxygen availability in tissues which causes cell injury by reducing aerobic oxidative respiration.

63
Q

The effects of hypoxia can be what 2 things

A

Reversible
Result in adaptation

64
Q

If tissue hypoxia is prolonged it can cause cell death of which type

A

Necrosis

65
Q

What causes hypoxia

A

Inadequate blood oxygenation
-Cardio-respiratory failure
-Lung disease
-Low ambient oxygen (e.g. altitude)

Decreased blood oxygen-carrying capacity
-Anaemia
-Carbon monoxide poisoning

Ischaemia

66
Q

What is ischaemia most commonly caused by

A

Obstruction to arterial supply by mechanisms such as severe atherosclerosis, thrombosis and embolism

67
Q

What is another thing that causes ischaemia but isn’t very common

A

Obstruction to venous outflow

68
Q

Non-ischaemic (generalised) hypoxia impairs what

A

Oxygen supply only
Other metabolites still supplied e.g. glucose

69
Q

Ischaemia impairs what

A
  • decreases supply of metabolites including glucose
  • Glycolytic anaerobic respiration fails due to lack of glucose
  • build up of metabolites impairs anaerobic respiration further
70
Q

Out of non-ischaemic (generalised) hypoxia and ischaemia, which one is worse and why

A

Ischaemia
Injures tissues faster/more severely

71
Q

When is cell injury reversible

A

If limited/short duration

72
Q

what can be therapeutic to ischaemic tissues

A

Rapid restoration of blood flow

73
Q

When is cell injury irreversible

A

If prolonged/sustained

74
Q

What is the type of cell death in ischaemic injury

A

Necrosis

75
Q

What is tissue necrosis called when caused by ischaemia

A

Infarction

76
Q

Define infarction

A

Tissue necrosis as a consequence of ischaemia (i.e. ischaemic necrosis)

77
Q

Is treating ischaemia through tissue repercussion a good thing

A

Yes but only if ischaemia is reversible (e.g. rapid PCI for MI/thrombolysis for stroke)

78
Q

what happens if ischaemia is treated and it isn’t reversible

A

Permanent damage
Repercussions of infarcted tissues will have no effect

79
Q

Is reperfusion of non-infarcted but ischaemic tissues always good?

A

No

80
Q

What is ischameia-(reperfusion) injury

A

Generation of reactive oxygen species by sudden reperfusion of ischaemic (dysfunctional) tissues

Reactive oxygen species generated by inflammatory cells cause further cell damage

81
Q

Generally, which is better from reperfusion and infarction

A

Reperfusion

82
Q

Infarction can be classified morphologically by what

A

Colour

83
Q

What are the two types of infarction

A

RED INFARCTION (HAEMORRHAGIC)
WHITE INFARCTION (ANAEMIC)

84
Q

When does red infarction occur

A

Dual blood supply/venous infarction

85
Q

When does white infarction occur

A

Single blood supply hence totally cut off

86
Q

Why are most infarcts wedge shaped

A
  • Vascular supply is “up-steam” or “proximal” in the tissue.
  • Deeper into the tissue the vascular branches expand
  • If obstruction occurs at an upstream point, the entire down-stream area will be infarcted
87
Q

What is the type of necrosis usually seen in infarction

A

Coagulative necrosis

88
Q

What type if necrosis is seen in brain infarction
Why

A

Colliquative necrosis
No connective tissue framework

89
Q

If a person dies suddenly (e.g. massive heart attack) what do you see in the tissues?

A

~ NOTHING
- NO TIME TO DEVELOP HEMORRHAGE / INFLAMMATORY RESPONSE INTO THE INFARCTED TISSUES

90
Q

Describe the morphological GROSS and MICROSCOPIC features in myocardial infarction after
A. <24 hours
B. 1-2 days
C. 3-4 daysD.
D. 1-3 weeks
E. 3-6 weeks

A

Gross
A. Normal
B. Pale red/oedematous
C. Yellow with haemorrhaging edge
D. Pale/thin
E. Dense fibrous scar

Microscopic
A. Normal
B. Oedema with early neutrophil infiltration
C. Coagulative necrosis with macrophage infiltration
D. Granulation tissue formation
E. Dense fibrous scar

91
Q

What is gangrene

A

Infarction of entire portion of limb (or organ)

92
Q

What is dry gangrene

A

Ischaemic coagulative necrosis only (sterile)

93
Q

What is wet gangrene

A

Gangrene with superimposed infection

94
Q

What is gas gangrene

A

Superimposed infection with gas producing organism e.g. clostridium perferinges

95
Q

Ischaemic necrosis is the same thing as what

A

Infarction

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