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Phase 2A Mehdi > THROMBOSIS, EMBOLISM, ISCHAEMIA & INFARCTION > Flashcards

THROMBOSIS, EMBOLISM, ISCHAEMIA & INFARCTION Flashcards

1
Q

What is thrombosis

A

Solidification of blood contents that form within the vascular system during life

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2
Q

What is the difference between thrombosis and clot

A

Clot is outside vascular system/after death

Thrombosis is inside vascular system/during life

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3
Q

What is laminar flow

A

Cells travel in one direction centerally

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4
Q

Why doesn’t a thrombus form all the time

A

Cells have laminar flow (do not touch sides)

HEALTHY Endothelial cells are NOT sticky

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5
Q

What are platelets derived from

A

Megakaryocytes in the bone marrow

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6
Q

What do platelets contain

A 
No nucleus
Alpha granules (for platelet to wall adhesion) 
Dense granules (cause aggregation)
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7
Q

What substances are found in alpha platelet granules

A

Fibrinogen
Fibronectin
Platelet growth factor

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8
Q

What substances are found in dense platelet granules

A

ADP

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9
Q

When are platelets activated to release granules

A

When platelets make contact with collagen

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10
Q

What happens when platelets make contact with collagen

A

Platelet shape change
Extend pseudopodia
Granule content release
Platelets form a mass to cover endothelium

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11
Q

How is a thrombus formed

A
  • Platelet aggregation - more platelets stick together by chemicals and start of clotting cascade (positive feedback)
  • Fibrin mesh formation - trap red blood cells
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12
Q

What three things can cause thrombosis

A

Change in….

  • Vessel wall
  • blood flow
  • blood contents
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13
Q

What changes does and atheromatous plaque cause

A

Change in….

  • vessel wall
  • blood flow
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14
Q

Describe the process of arterial thrombosis

A
  • Plaque has raised fatty streak in intima
  • Plaque grows and protrudes (turbulent blood flow)
  • Turbulence = loss of intimal cells and exposed plaque to blood
  • Fibrin deposition and platelet clumping
  • Platelet GF causes proliferation of smooth muscle cell in plaque
  • Platelet layer forms = red blood cells trapped = more turbulence = more platelet deposition
  • Laminar flow is disrupted
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15
Q

What is propogation

A

When the thrombi grows in the direction of blood flow

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16
Q

Why don’t atheroma form in veins

A

Low blood pressure in veins

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17
Q

Where does most turbulence occur in arterial thrombosis

A

Downstream side of arterial thrombus

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18
Q

Where does most turbulence occur in venous thrombosis

A

Upstream side of venous thrombus

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19
Q

Where do venous thrombi begin

A

At the valves due to turbulence from protruding

Valves can also be damaged by trauma, stasis or occlusion

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20
Q

How do thrombi grow in young active individuals with no pre disposition

A

By propagation with successive deposition

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21
Q

Why does thrombosis become more likely during surgery or after MI

A

Blood pressure drops

More contact time of slow blood flow with damaged vein valves

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22
Q

What can cause Deep vein thrombosis

A

Immobilisation of the leg most importantly muscle contraction and relaxation of calf muscle

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23
Q

What are the clinical effects of arterial thrombosis

A

1) Loss of pulse distal to thrombus
2) Area becomes cold, pail and painful
3) Tissue death and gangrene

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24
Q

What are the clinical effects of venous thrombosis

A

Tender area due to ischaemia
Red area due to no blood drainage
Swollen area

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25
Q

What are the 4 fates of thrombi

A

Lysis and resolution
Organisation - macrophage clear thrombus, fibroblast replace it with collagen = slight vessel narrowing
Recanilisation - Intimal cells proliferate, capillaries sprout and fuse to form larger vessels = functional
Embolism - Thrombus fragments break into circulation

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26
Q

How does aspirin prevent clotting

A

Inhibit platelet aggregation = prevent thrombosis

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27
Q

How does warfarin work

A

Inhibit Vitamin K (clotting factor) - severe cases

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28
Q

What is an embolus

A

A mass of material in the vascular system that can lodge in vessels and block the lumen

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29
Q

Cause of embolus

A

Air - IV fluid/bloods
Cholesterol crystals - plaques
Tumour amniotic fluid - pregnant women with rapid labour
Fat - sever trauma

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30
Q

What causes a pulmonary embolism

A

Embolus to venous system to Vena Cava to Pulmonary arteries

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31
Q

Why can’t an embolus travel through arterial circulation

A

Lung blood vessels split to capillary size (too small for embolus)

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32
Q

What is the exception of a pulmonary embolus entering the arterial side

A

Paradoxical Embolus- perforated septum in the heart allowing arterial-venous communication

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33
Q

What is the effect of a small pulmonary embolus

A

Can go unnoticed and be lysed in the lung

Can be organised and cause permanent minor respiratory deficiency

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34
Q

What is Idiopathic pulmonary hypertension

A

Prolonged damage from small embolus

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35
Q

What is the effect of a large pulmonary embolus

A

Can cause acute respiratory/cardiac problems that can resolve slowly
Can cause chest pain/ breath shortness from infarcted lung

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36
Q

What is the effect of massive pulmonary embolus

A

Sudden death

Usually long thrombi from leg veins which affect the bifurcation of pulmonary arteries

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37
Q

Where can arterial embolus travel

A

Anywhere downstream in the systemic circulation

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38
Q

Where can cholesterol crystals from atheromatous plaques travel

A

Any lower limb and renal arteries

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39
Q

Where do most systemic embolisms originate from

A

Heart

Atheromatous plaque

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40
Q

Why can thrombi form on dead cardiac muscle

A

After MI, the muscle loses its normal endothelial lining so will expose its collagen to platelets = aggregation

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41
Q

How can atrial fibrillation cause thrombosis

A

Blood stagnates in atrial appendages

When normal rhythm returns, the emboli may break off

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42
Q

What is Ischaemia

A

Reduction of blood flow to tissue due to constriction/blockage of supplying vessel

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43
Q

When can Ischaemia br reversed

A

After brief ischaemic periods

If the tissue has low metabolic demands (myocytes and neurones are most vulnerable)

44
Q

What is Infarction

A

Necrosis of an organ due to artery obstruction

45
Q

What typically causes Infarction

A

Thrombosis blocking arteries

46
Q

What organs have dual arterial supply

A

Liver - portal venous and hepatic artery
Lung - pulmonary venous and bronchial artery
Brain - Circle of willis (many arteries)

47
Q

What is reperfusion injury

A

Tissue damage occurs during reperfusion and not during ischaemic period as damage is oxygen dependant

48
Q

What causes damage during reperfusion

A

Damaged cell membrane transport triggers activation of oxygen-dependant free radical systems
Dead cells are cleared by oxygen free radicals
Neutrophils and macrophages also release oxygen free radicals and cause more damage by removing the cells = necrosis

49
Q

What is gangrene

A

When whole areas of a limb or a region of the gut have their arterial
supply cut off and large areas of mixed tissue die in bulk

50
Q

What are the two types of gangrene

A

Dry

Wet

51
Q

What is dry gangrene

A

Tissue dies and healing occurs on top

Dead area drops off

52
Q

What is wet gangrene

A

Bacterial infection causes spread of gangrene proximally and patient dies from sepsis

53
Q

What is capillary ischaemia

A

Frostbite can cause infarction as capillaries undergo ischaemia

54
Q

What is Disseminated Intravascular Coagulation

A

Disease and therapy can disturb the balance of thrombotic and thrombolytic mechanisms
Thrombosis can be activated without counterbalance = thrombi throughout the body and bleeding due to clotting factor consumption

55
Q

What is a watershed area

A

Tissue at the boundary between the territories of two arteries
This area is prone to infarction

56
Q

What are examples of watershed areas

A

Colon splenic flexure - between SMA and IMA
Cerebral hemispheres - between major cerebral arteries
Myocardium - between subendocardial myocardium and coronary arteries

57
Q

Why is the distal component of portal system vulnerable to ischaemic attack

A

Blood passed through first set of capillaries
Drop in intravascular pressure and oxygen saturation
Tissue supplied by the 2nd set of capillaries likely to ischaemia

58
Q

What are examples of already perfused portal tissues

A

Anterior pituitary - blood already perfused hypothalamus
Renal tubular epithelium - blood already perfused by glomerular capillaries
Exocrine pancreas - blood already perfused Islets of Langerhans

59
Q

What are non-thrombi causes of ischaemia

A 
Spasm
External compression
Steal syndromes
Hyperviscosity
Vasculitis
60
Q

How can spasms cause ischaemia

A
  • Smooth muscle spasm (transient arterial narrowing)
  • cellular injury = decrease in NO3
  • Coronary artery spasm = angina
61
Q

What can spasms be treated with

A

Glyceryltrinitrate

62
Q

How can external compression cause ischaemia

A
  • Blood vessels can be partially occluded by compression

- This can be done intentionally by ligation to prevent haemorrhage

63
Q

Why are veins most susceptible to external compression

A

thin walls
low intraluminal pressure
occurs mostly in strangulated hernias, testicular tortion, ovarian tortion

64
Q

When do steal syndromes occur

A

When blood is diverted from an area of atheromatous making that vessel ischaemic

65
Q

what causes hyperviscosity

A

In myeloma(tumour of plasma cells) high conc. of antibodies causes hyper viscosity

66
Q

What is vasculitis

A

Inflammation of vessel wall narrows lumen

67
Q

What is atherosclerosis

A

The formation of plaques in the aortic intima and coronary arteries

68
Q

When is atherosclerosis clinically important

A

The formation of occlusive thrombosis on a disrupted plaque

69
Q

What is the result of atherosclerosis

A 
Cerebral infarction
Carotid atheroma
Myocardial Infarction
Aortic aneurysm (rupture)
Peripheral vascular disease
Gangrene
70
Q

What is a fatty streak

A

The earliest significant lesion

Yellow linear elevation made of lipid-laden macrophages

71
Q

What is a plaque

A

A lesion with a central lipid core with a fibrous cap covered by endothelium

72
Q

What provides structural strength to the plaque

A

Collagen produced by Smooth muscle cells give strength

73
Q

What cells arise from arterial endothelium

A

macrophages
T-lymphopcytes
mast cells

74
Q

What are foam cells

A

Macrophages with oxidised lipoproteins

75
Q

What is dystrophic calcification

A

It acts as a amrker of late atherosclerosis in angiograms and CT scans

76
Q

Where do plaques tend to form

A

Bifurcations and branching points

77
Q

What are the main risk factors of atherosclerosis

A

Hypercholesterolaemia (lipids directly damage endothelial cells)
Smoking (nicotine damages endothelium and increase blood pressure)
Hypertension
Diabetes
Male gender
Increasing age

78
Q

What are the 2 steps in plaque formation

A
  • Endothelium damage

- Tissue response

79
Q

What changes take place in endothelial cells at plaque formation sites

A
  • monocytes have increased expression of cell adhesion
  • macromolecules (LDL) have high permeability
  • Increased thrombogenicity
80
Q

How do plaques develop

A
  • Endothelial functional change
  • Inflammatory cells and lipids enter intimal layer
  • Macrophages and Tcells enter area to build plaque
  • Foam cells phagocytose LDL and apoptose increasing lipid content in plaque
81
Q

How does the fibrous cap form

A

Platelet derived growth factor stimulate proliferation of intimal SMC and synthesise collagen, elastin and mucopolysaccharide

82
Q

What secretes growth factors

A

platelets
injured endothelium
macrophages
SMC

83
Q

What are the causes of atherosclerotic clinical manifestations

A
  • Plaque stenosis
  • Acute occlusion
  • Distal arterial bed embolisation
  • Ruptured abdominal aneurysm
84
Q

Describe plaque stenosis

A

Lumen narrowing

  • minor = reversible ischaemia during activity
  • major = Ischaemic pain during rest
85
Q

What increases the rate of plaque stenosis

A

Intraplaque haemorrhages

86
Q

What causes acute occlusion

A

Plaque rupture = exposed collagen/lipid
coagulation cascade = occlusion
Total occlusion? = irreversible ischaemia causing infarction

87
Q

Describe embolisation of the distal arterial bed

A
  • small emboli detach
  • embolise to the distal arterial bed
  • occlude small vessels = small infarctions
88
Q

Describe ruptured abdominal atherosclerotic aneurysm

A

Rupture can cause retroperitoneal haemorrhage and death

89
Q

State some atherosclerosis preventative measures

A 
Smoking cessation
Blood pressure control
Weight reduction
Low dose aspirin (platelet aggregation inhibitor)
Statins (cholesterol reducing)
90
Q

What is an aneurysm

A

Localised permanent dilation(weakened) in the vascular tree

91
Q

What is the result of an atherosclerotic aortic aneurysm

A

Impaired blood flow to the lower limbs

They can rupture

92
Q

What is aortic dissection

A

Blood is forced through a tear in the aortic intima into the aortic media to make a blood filled space

93
Q

What is fatal haemopericardium

A

When blood is tracked back into the pericardial cavity

94
Q

What is a berry aneurysm

A
  • In the Circle of Willis (branches)
  • Normal arterial wall replaced with fibrous tissue
  • Common in young hypertensive patients
  • Can cause subarachnoid haemorrhage
95
Q

What is a stroke

A

Sudden disturbance of CNS functions from vascular disease

96
Q

What is a transient ischaemic attack

A
  • lasts <24 hours
  • complete recovery
  • can cause subsequent attacks
97
Q

Where do most cerebral infarctions occur

A

Internal carotid territory (middle cerebral artery)

98
Q

What are the causes of Cerebral infarction

A
  • Arterial thrombosis from atheroma in intracranial/extracranial arteries supplying CNS
  • Embolic arterial occlusion in extracranial vessels
  • Head injury = Cerebral hypoxia/vascular occlusions/ rupture
  • Saccular aneurysm = subarachnoid haemorrhage = vascular spasm
  • Reduction in cerebral blood flow(cardiac arrest)
  • Reduction in arterial oxygenation(respiratory arrest)
  • Venous thrombosis (local sepsis)
99
Q

What are the 2 types of intracranial haemorrhages

A

Intracerebral

Subarachnoid

100
Q

Where does intracerebral haemorrhage occur

A

Basal ganglia
brainstem
cerebellum
cerebral cortex

101
Q

How does intracerebral haemorrhage come about

A
  • Follows rupture of lenticulostriate branch of Middle cerebral artery
  • Haematoma acts as a legion
  • Rapid increase of intracranial pressure and herniation
102
Q

Where do subarachnoid haemorrhages occur

A

Between arachnoid and Pia Mata of cranial meninges

103
Q

What happens during a subarachnoid haemorrhage

A

Increase in pressure on the brain and intracranial vessels

104
Q

What are the causes of subarachnoid haemorrhages

A
  • Saccular aneurysm in circle of willis
  • Trauma
  • Hypertensive haemorrhage
  • Vasculitis
  • Rumours
  • Coagulation disorders
105
Q

What is vasculitis

A

Inflammation of the blood vessels

Phase 2A Mehdi (6 decks)

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