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YR 3 - Illness and Wellbeing > Pathology - Haemodynamic Disorders > Flashcards

Pathology - Haemodynamic Disorders Flashcards

1
Q

define haemostasis

A

the process by which blood clots form at sites of blood vessel wall damage

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2
Q

two types of haemostasis?

A

primary and secondary

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3
Q

what is primary haemostasis?

A

the platelet plug forms by exposing collagen to VWF

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4
Q

what is secondary haemostasis?

A

fibrin meshwork formatin via exposure of tissue factor

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5
Q

the haemostasis sequence (4)

A

vasoconstriction
primary haemostasis
secondary haemostasis
clot stabilisation/resorption

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6
Q

why do vessels vasoconstrict?

A

reduce the blood flow to minimise blood loss

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7
Q

how is vasoconstriction regulated?

A

neurogenic factor - endothelin

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8
Q

where do you find Von Willebrand Factors?

A

in the blood plasma

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9
Q

how does primary haemostasis occur? (7)

A
  1. endothelial disruption
  2. collagen and VWF get exposed
  3. platelets in the blood bind to WBF
    = via glycoprotein 1b
  4. platelets change shape = spiky for SA
  5. platelets secrete granules
    = ADP and Thrombin A2
  6. more platelets recruited
    = aggregation for plug
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10
Q

how does secondary haemostasis occur?

A
  1. tissue factors are exposed
  2. coagulation cascade is activated
  3. extrinsic pathway
    - factor 7 activated
  4. thrombin formation
  5. thrombin cleaves soluble fibrinogen into fibrin meshwork
  6. thrombin activates more platelets
  7. RBC trap within the clot
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11
Q

what is Fibrinolysis?

A

the enzymatic breakdown of fibrin in blood clots

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12
Q

how is fibrinolysis activated?

A

tissue plasminogen activator - t-PA
secreted by endothelial cells

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13
Q

what is t-PA?

A

tissue plasminogen activator

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14
Q

what is the role of t-PA?

A

catalyse plasminogen into plasmin
plasmin breaks down fibrin

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15
Q

what do normal endothelial cells inhibit and promote?

A

inhibit coagulation cascade
inhibit platelet aggregation

promote fibrinolysis

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16
Q

5 Risk factors for endothelial damage.

A

hyperlipidaemia
diabetes
hypertension
toxins
smoking

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17
Q

what are the steps of atherosclerosis development? (8)

A
  • endothelial damage
  • increased permeability
  • low density lipoprotein accumulates, platelets and monocyte adhesion
  • macrophage migrate and activate
  • smooth muscle cells recruitment
  • lipid uptake and T cell activation
  • chronic inflammation
  • left with lesion, smooth muscle cells, lipid, macrophages with fibrous cap
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18
Q

what is critical stenosis?

A

if the atherosclerotic plaque grows and grows
and leads to ischemia

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19
Q

how can atherosclerosis lead to an aneurysm and rupture?

A

if there is muscle weakening

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20
Q

what happens if atherosclerotic plaque ruptures?

A

VWF factor, tissue factor can be exposed
- lead to thrombosis
- activate primary and secondary haemostasis

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21
Q

how can atherosclerosis lead to myocardial infarction?

A

rupture of atherosclerotic plaque
thrombosis
blocks blood supply to the heart
no oxygen

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22
Q

define thrombosis

A

the inappropriate activation of a normal haemostatic mechanism which results in the formation of a thrombus

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23
Q

define thrombus

A

a structured solid mass or plug of blood constituents formed within the heart or blood vessels

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24
Q

What are the 3 Factors of Thrombosis

A

Virchow’s Triad
- endothelial injury
- hypercoagulability
- abnormal blood flow

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25
Q

what constitutes virchows triad?

A
  • endothelial injury
  • hypercoagulability
  • abnormal blood flow
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26
Q

Noxious Stimuli can be Pro-Thrombotic and lead to Endothelial Injury. Give 5 noxious stimuli.

A
  • physical injury
  • infection
  • abnormal blood flow
  • toxins - smoking
  • inflammatory mediators
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27
Q

give 2 effects of a dysfunctional endothelial cells

A
  1. pro-coagulant effects
  2. anti-fibrinolysis
    - decrease t-PA
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28
Q

give 3 proteinsthat a pro-coagulant decreases

A

decrease in:
thrombomodulin
protein C
tissue factor protein inhibitor

= all = anticoagulants

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29
Q

what are the 2 types of blood flow?

A

turbulence
stasis

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30
Q

3 Effects of Abnormal Blood Flow.

A
  1. activate endothelial cells
    - become pro-thrombotic
  2. disrupt normal flow
    - platelets interact with endothelium
  3. prevents dilution of clotting factors
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31
Q

Define Hypercoagulability

A

the abnormal tendency for blood to clot

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32
Q

What is the most common genetic cause for hypercoagulability?

A

mutation in factor V
= factor V Leiden

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33
Q

Name 9 secondary risk factors for hypercoagulability.

A
  • immobilisation
  • myocardial infarction
  • atrial fibrillation
  • prosthetic cardiac valves
  • tissue injury
  • cancer
  • heparin-induced thrombocytopenia
  • antiphospholipid antibody syndrome
  • disseminated intravascular coagulation
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34
Q

What is Venous Thrombosis also known as?

A

Phlebothrombosis

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35
Q

what do venous emboli lead do?

A

pulmonary embolism

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36
Q

What is the Origin for Pulmonary Embolism?

A

DVT

37
Q

Describe the steps of DVT to pulomary embolism

A

dvt fragments
embolus enters inferior vena cava
passes through right heart
stops in the pulmonary vessels

38
Q

what is the dominant mechanism for Venous Thrombosis/Phlebothrombosis?

A

stasis

39
Q

Where is Venous Thrombosis/Phlebothrombosis common?

A

deep veins of the leg DVT

40
Q

what is the classical history of pulmonary embolism? (4)

A
  • post hip replacement - immobile
  • dyspnoea - shortness of breath
  • hypoxia
  • tachycardia
41
Q

What is Arterial Thrombosis also known as?

A

Cardiac or Systemic Thrombosis

42
Q

what are the 2 dominant mechanisms of arterial thrombosis?

A

turbulence and or endothelial injury of the heart

43
Q

what 4 things can happen to a clot after thrombosis?

A
  1. propagation
    - gets larger by accumulation of fibrin/platelets
  2. dissolution via fibrinolysis
  3. organisation and recanalisation
  4. embolisation
44
Q

what happens to a clot if it organises and recanalises?

A

it has an ingrowth of endothelial cells
forms new blood vessel channels
blood flows through

45
Q

define embolisation

A

the 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

46
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

47
Q

what are almost all emboli?

A

all emboli are thrombosis-emboli

48
Q

what is an atherosclerotic emboli?

A

bits of atherosclerotic plaque are thrown into the blood vessel
- seen in aortic aneurysms

49
Q

apart from thromboembolic, what are rare 6 types of emboli?

A
  • atherosclerotic
  • infective
  • tumour
  • gas
  • amniotic
  • fat
50
Q

what are infective emboli?

A

lumps of infection break off
- often from heart valves

51
Q

what are gas embolisms?

A

from rapid decompressions during diving
- develop nitrogen bubbles into blood

52
Q

what is amniotic fluid embolism?

A

amniotic fluid goes into the mothers blood stream

53
Q

what is fat embolism?

A

from trauma

fat can break off and embolism

54
Q

what are the effects of large pulmonary vessels getting blocked?

A

saddle embolus
death

55
Q

what % of plumonary flow leads to death if blocked?

A

60%

56
Q

can a pulmonary embolism lead to instant death?

A

yes

57
Q

what are the effects of small vessels getting blocked from pulmonary embolism?

A

dyspnoae and pleuritic chest pain - pain from inspiration

58
Q

what % of small vessel obstructions are asymptomatic from pulmonary embolisms?

A

60-80%

59
Q

80% of Systemic Thromboembolisms come from?

A

intra-cardiac mural thrombi

60
Q

What can be the Effect of Arterial Thromboembolism?

A

ischemic injury
- limbs 75%
- brain 10%
- other viscera 15%

61
Q

What is a Paradoxical Embolism?

A

embolus goes from the venous circulation straight to the systemic circulation to the rest of the body - brain, limbs or organs

62
Q

How does a Paradoxical Embolism occur?

A

if a person has a heart defect or hole in the heart

63
Q

What is the Route of a Paradoxical Embolism compared to a Regular Embolism in the Heart?

A

Regular:
- embolus arises from venous circulation
- through vena cava
- into right side of the heart
- into pulmonary circulation

Paradoxical:
- embolus goes from the venous circulation straight to the systemic circulation to the rest of the body - brain, limbs or organs

64
Q

What is Hypoxia?

A

a state of reduced oxygen availability which causes cell injury by reducing aerobic oxidative respiration

65
Q

Two Paths of Hypoxia to take

A

reversible
adaption

  • if injury is not sustained
66
Q

what happens if hypoxia is prolonged?

A

cell death - necrosis

67
Q

What causes Hypoxia?

A
  • inadequate blood oxygenation = generalised
  • decreased blood oxygen-carrying capacity = generalised
68
Q

How do you get Inadequate Blood Oxygenation?

A
  • cardio respiratory failure
  • lung failure
  • low ambient oxygen e.g. altitude
69
Q

how can a decrease in blood oxygen carrying capacity occur? (2)

A
  • anaemia
  • carbon monoxide poisoning
70
Q

Define Ischaemia

A

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

71
Q

how can ischaemia arise? (3)

A
  • severe atherosclerosis
  • thrombosis
  • embolism
72
Q

can ischaemia be reversible?

A

ONLY IF SHORT DURATION AND RAPID RESTORATION OF BLOOD FLOW

73
Q

what type of cell death occurs in ischaemia?

A

necrosis

74
Q

what is tissue necrosis when caused by ischaemia?

A

infarction

75
Q

define infarction

A

tissue necrosis as a consequence of ischaemia

76
Q

what is Ischaemia Reperfusion Injury?

A

if you reperfuse ischamic, dysfunctional tissues with blood
- generates ROS from inflam cells
= more cell damage

77
Q

In Which Two Ways can Infarction be Classified according to Morphology?

A

colour
shape

78
Q

What are the two types of infarction?

A

red - haemorrhagic
white - anaemia

79
Q

How does Red Infarction Arise?

A

dual blood supply e.g. lungs
tissue is flooded with blood = red

venous infarction
blockage with tissue is flooded with blood

80
Q

How does White Infarction Arise?

A

single blood supply cut off = white

81
Q

Why are Infarctions Wedge-Shaped?

A

when obstruction occurs at an up-stream point

  • the down stream branches will be infarcted

= wedge shaped

82
Q

What is the Most Common Type of Necrosis in Infarction?

A

Coagulative
- good connective tissue
- framework is kept
e.g. kidney or heart

83
Q

What Necrosis happens in the Brain?

A

Colliquative

84
Q

If a person suddenly dies from heart attack, what would you see in the heart tissue?

A

nothing
no time to develop haemorrhage or inflammatory response to infarcted tissue

85
Q

How does the heart appear less than 24 hrs after a MI?

A

appears normal

86
Q

How does the heart appear 1-2 days after a MI?

A

pale red
oedema
neutrophil infiltration

87
Q

How does the heart appear 3-4 days after a MI?

A

chronic inflammation overtakes

yellow
haemorrhagic edge
coagulative necrosis
macrophage infiltration

88
Q

How does the heart appear 1-3 weeks after a MI?

A

pale and thin
granulation tissue formation

89
Q

How does the heart appear 3-6 weeks after a MI?

A

dense fibrous scar

YR 3 - Illness and Wellbeing (31 decks)

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