THROMBOSIS, EMBOLISM, ISCHAEMIA & INFARCTION Flashcards
(105 cards)
1
Q
What is thrombosis
A
Solidification of blood contents that form within the vascular system during life
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
3
Q
What is laminar flow
A
Cells travel in one direction centerally
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
5
Q
What are platelets derived from
A
Megakaryocytes in the bone marrow
6
Q
What do platelets contain
A
No nucleus Alpha granules (for platelet to wall adhesion) Dense granules (cause aggregation)
7
Q
What substances are found in alpha platelet granules
A
Fibrinogen
Fibronectin
Platelet growth factor
8
Q
What substances are found in dense platelet granules
A
ADP
9
Q
When are platelets activated to release granules
A
When platelets make contact with collagen
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
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
12
Q
What three things can cause thrombosis
A
Change in….
- Vessel wall
- blood flow
- blood contents
13
Q
What changes does and atheromatous plaque cause
A
Change in….
- vessel wall
- blood flow
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
15
Q
What is propogation
A
When the thrombi grows in the direction of blood flow
16
Q
Why don’t atheroma form in veins
A
Low blood pressure in veins
17
Q
Where does most turbulence occur in arterial thrombosis
A
Downstream side of arterial thrombus
18
Q
Where does most turbulence occur in venous thrombosis
A
Upstream side of venous thrombus
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
20
Q
How do thrombi grow in young active individuals with no pre disposition
A
By propagation with successive deposition
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
22
Q
What can cause Deep vein thrombosis
A
Immobilisation of the leg most importantly muscle contraction and relaxation of calf muscle
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
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
25
What are the 4 fates of thrombi
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
26
How does aspirin prevent clotting
Inhibit platelet aggregation = prevent thrombosis
27
How does warfarin work
Inhibit Vitamin K (clotting factor) - severe cases
28
What is an embolus
A mass of material in the vascular system that can lodge in vessels and block the lumen
29
Cause of embolus
Air - IV fluid/bloods
Cholesterol crystals - plaques
Tumour amniotic fluid - pregnant women with rapid labour
Fat - sever trauma
30
What causes a pulmonary embolism
Embolus to venous system to Vena Cava to Pulmonary arteries
31
Why can't an embolus travel through arterial circulation
Lung blood vessels split to capillary size (too small for embolus)
32
What is the exception of a pulmonary embolus entering the arterial side
Paradoxical Embolus- perforated septum in the heart allowing arterial-venous communication
33
What is the effect of a small pulmonary embolus
Can go unnoticed and be lysed in the lung
| Can be organised and cause permanent minor respiratory deficiency
34
What is Idiopathic pulmonary hypertension
Prolonged damage from small embolus
35
What is the effect of a large pulmonary embolus
Can cause acute respiratory/cardiac problems that can resolve slowly
Can cause chest pain/ breath shortness from infarcted lung
36
What is the effect of massive pulmonary embolus
Sudden death
| Usually long thrombi from leg veins which affect the bifurcation of pulmonary arteries
37
Where can arterial embolus travel
Anywhere downstream in the systemic circulation
38
Where can cholesterol crystals from atheromatous plaques travel
Any lower limb and renal arteries
39
Where do most systemic embolisms originate from
Heart
| Atheromatous plaque
40
Why can thrombi form on dead cardiac muscle
After MI, the muscle loses its normal endothelial lining so will expose its collagen to platelets = aggregation
41
How can atrial fibrillation cause thrombosis
Blood stagnates in atrial appendages
| When normal rhythm returns, the emboli may break off
42
What is Ischaemia
Reduction of blood flow to tissue due to constriction/blockage of supplying vessel
43
When can Ischaemia br reversed
After brief ischaemic periods
| If the tissue has low metabolic demands (myocytes and neurones are most vulnerable)
44
What is Infarction
Necrosis of an organ due to artery obstruction
45
What typically causes Infarction
Thrombosis blocking arteries
46
What organs have dual arterial supply
Liver - portal venous and hepatic artery
Lung - pulmonary venous and bronchial artery
Brain - Circle of willis (many arteries)
47
What is reperfusion injury
Tissue damage occurs during reperfusion and not during ischaemic period as damage is oxygen dependant
48
What causes damage during reperfusion
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
What is gangrene
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
What are the two types of gangrene
Dry
| Wet
51
What is dry gangrene
Tissue dies and healing occurs on top
| Dead area drops off
52
What is wet gangrene
Bacterial infection causes spread of gangrene proximally and patient dies from sepsis
53
What is capillary ischaemia
Frostbite can cause infarction as capillaries undergo ischaemia
54
What is Disseminated Intravascular Coagulation
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
What is a watershed area
Tissue at the boundary between the territories of two arteries
This area is prone to infarction
56
What are examples of watershed areas
Colon splenic flexure - between SMA and IMA
Cerebral hemispheres - between major cerebral arteries
Myocardium - between subendocardial myocardium and coronary arteries
57
Why is the distal component of portal system vulnerable to ischaemic attack
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
What are examples of already perfused portal tissues
Anterior pituitary - blood already perfused hypothalamus
Renal tubular epithelium - blood already perfused by glomerular capillaries
Exocrine pancreas - blood already perfused Islets of Langerhans
59
What are non-thrombi causes of ischaemia
```
Spasm
External compression
Steal syndromes
Hyperviscosity
Vasculitis
```
60
How can spasms cause ischaemia
- Smooth muscle spasm (transient arterial narrowing)
- cellular injury = decrease in NO3
- Coronary artery spasm = angina
61
What can spasms be treated with
Glyceryltrinitrate
62
How can external compression cause ischaemia
- Blood vessels can be partially occluded by compression
| - This can be done intentionally by ligation to prevent haemorrhage
63
Why are veins most susceptible to external compression
thin walls
low intraluminal pressure
occurs mostly in strangulated hernias, testicular tortion, ovarian tortion
64
When do steal syndromes occur
When blood is diverted from an area of atheromatous making that vessel ischaemic
65
what causes hyperviscosity
In myeloma(tumour of plasma cells) high conc. of antibodies causes hyper viscosity
66
What is vasculitis
Inflammation of vessel wall narrows lumen
67
What is atherosclerosis
The formation of plaques in the aortic intima and coronary arteries
68
When is atherosclerosis clinically important
The formation of occlusive thrombosis on a disrupted plaque
69
What is the result of atherosclerosis
```
Cerebral infarction
Carotid atheroma
Myocardial Infarction
Aortic aneurysm (rupture)
Peripheral vascular disease
Gangrene
```
70
What is a fatty streak
The earliest significant lesion
| Yellow linear elevation made of lipid-laden macrophages
71
What is a plaque
A lesion with a central lipid core with a fibrous cap covered by endothelium
72
What provides structural strength to the plaque
Collagen produced by Smooth muscle cells give strength
73
What cells arise from arterial endothelium
macrophages
T-lymphopcytes
mast cells
74
What are foam cells
Macrophages with oxidised lipoproteins
75
What is dystrophic calcification
It acts as a amrker of late atherosclerosis in angiograms and CT scans
76
Where do plaques tend to form
Bifurcations and branching points
77
What are the main risk factors of atherosclerosis
Hypercholesterolaemia (lipids directly damage endothelial cells)
Smoking (nicotine damages endothelium and increase blood pressure)
Hypertension
Diabetes
Male gender
Increasing age
78
What are the 2 steps in plaque formation
- Endothelium damage
| - Tissue response
79
What changes take place in endothelial cells at plaque formation sites
- monocytes have increased expression of cell adhesion
- macromolecules (LDL) have high permeability
- Increased thrombogenicity
80
How do plaques develop
- 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
How does the fibrous cap form
Platelet derived growth factor stimulate proliferation of intimal SMC and synthesise collagen, elastin and mucopolysaccharide
82
What secretes growth factors
platelets
injured endothelium
macrophages
SMC
83
What are the causes of atherosclerotic clinical manifestations
- Plaque stenosis
- Acute occlusion
- Distal arterial bed embolisation
- Ruptured abdominal aneurysm
84
Describe plaque stenosis
Lumen narrowing
- minor = reversible ischaemia during activity
- major = Ischaemic pain during rest
85
What increases the rate of plaque stenosis
Intraplaque haemorrhages
86
What causes acute occlusion
Plaque rupture = exposed collagen/lipid
coagulation cascade = occlusion
Total occlusion? = irreversible ischaemia causing infarction
87
Describe embolisation of the distal arterial bed
- small emboli detach
- embolise to the distal arterial bed
- occlude small vessels = small infarctions
88
Describe ruptured abdominal atherosclerotic aneurysm
Rupture can cause retroperitoneal haemorrhage and death
89
State some atherosclerosis preventative measures
```
Smoking cessation
Blood pressure control
Weight reduction
Low dose aspirin (platelet aggregation inhibitor)
Statins (cholesterol reducing)
```
90
What is an aneurysm
Localised permanent dilation(weakened) in the vascular tree
91
What is the result of an atherosclerotic aortic aneurysm
Impaired blood flow to the lower limbs
| They can rupture
92
What is aortic dissection
Blood is forced through a tear in the aortic intima into the aortic media to make a blood filled space
93
What is fatal haemopericardium
When blood is tracked back into the pericardial cavity
94
What is a berry aneurysm
- In the Circle of Willis (branches)
- Normal arterial wall replaced with fibrous tissue
- Common in young hypertensive patients
- Can cause subarachnoid haemorrhage
95
What is a stroke
Sudden disturbance of CNS functions from vascular disease
96
What is a transient ischaemic attack
- lasts <24 hours
- complete recovery
- can cause subsequent attacks
97
Where do most cerebral infarctions occur
Internal carotid territory (middle cerebral artery)
98
What are the causes of Cerebral infarction
- 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
What are the 2 types of intracranial haemorrhages
Intracerebral
| Subarachnoid
100
Where does intracerebral haemorrhage occur
Basal ganglia
brainstem
cerebellum
cerebral cortex
101
How does intracerebral haemorrhage come about
- Follows rupture of lenticulostriate branch of Middle cerebral artery
- Haematoma acts as a legion
- Rapid increase of intracranial pressure and herniation
102
Where do subarachnoid haemorrhages occur
Between arachnoid and Pia Mata of cranial meninges
103
What happens during a subarachnoid haemorrhage
Increase in pressure on the brain and intracranial vessels
104
What are the causes of subarachnoid haemorrhages
- Saccular aneurysm in circle of willis
- Trauma
- Hypertensive haemorrhage
- Vasculitis
- Rumours
- Coagulation disorders
105
What is vasculitis
Inflammation of the blood vessels
