Atherosclerosis thrombosis and embolism Flashcards

we will cover atherosclerosis thrombosis and emboli types of risk factors development treatment prevention ischaemia and infarction shock (73 cards)

1
Q

describe the physiology of blood vessels and endothelial cells

A

inner layer: intima
middle media
outer- adventitia

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2
Q

what is the difference between the media in a vein and an artery

A

the media in the artery is much bigger diameter

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3
Q

what is the origin of endothelial cells

A

mesodermal origin

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4
Q

what are endothelial cells found

A

interior surface of blood vessels and the lymphatics and on the inside of the heart( called the endocardium)

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5
Q

what are endothelial cells called inside the heart

A

endocardium

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6
Q

what is the function of the endothelial cells

A

semi selective barrier function- allows WBC to move out to the area of infection (diapedesis)

  • angiogenesis
  • mediator of coagulation
  • blood pressure control
  • fluid filtration
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7
Q

what happens with prolonged inflammation to the endothelial cells

A

increased permeability and tissue swelling

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8
Q

what clotting factors do endothelial cells mediate

A

von willibrands factor- stabilises factor VIII which binds to collagen linking platelets
heparan sulphate- inactivates clotting cascade

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9
Q

what does heparan sulphate control

A

inactivates clotting cascade

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10
Q

which diseases is endothelial cell dysfunction

A

many diseases
septic shock
hypertension
behcets

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11
Q

how else can endothelial cell dysfunction arise

A

tobacco and air pollution

trans fat consumption

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12
Q

how can endothelial cell dysfunction improve

A

smoking cessation
weight loss
improved diet
exercise

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13
Q

what is a atheroma

A

is an accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries

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14
Q

what is atherosclerosis

A

the thickening and hardening of arterial walls as a consequence of atheroma

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15
Q

why do atheromas form and why in the arteries

A

due to chronic endothelial cell damage- in the arteries as BP is higher

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16
Q

how does an atheroma develop 11 steps

A
  1. chronic endothelial cell dysfuction
    2 endothelial dysfunction
    3 entrance of LDL in intimia
    4 lipid engulfed by macrophages
    5 flat yellow(fatty streak) early atheroma
    6 accumulation of lipids- in macrophages and smooth muscle wall
    7 raised yellow lipid plaque
    8 extracellular lipid deposits and collagen deposition and calcification
    9 fibrous cap over the lipid core(fibroatheroma)
    10 ulceration of plaque
    11 predisposition to thrombus formation- advanced complicated plaque
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17
Q

what are the risk factors for atheroma

A
high LDL/low HDL 
hypertension
diabetes 
sedentary lifestyle
obesity
smoking
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18
Q

what are the two forms of prevention for the formation of atherosclerosis

A

primary- risk factor modification

secondary- includes regulation medications such as aspirin and the prevention of the recurrence of events

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19
Q

when do early atheromas start forming

A

in your early 20s-30s

progressive

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20
Q

which medications can be used to stabilise the plaques and prevent rupture

A

statins

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21
Q

what medication can be used if the atheroma was to rupture

A

antithrombotic agents

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22
Q

which sites can be affected

A

aorta-
coronary artery
iliac and popliteal arteries
internal carotid arteries

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23
Q

what happens if the aorta is affected by atheroma

A

weakening of the aorta leading to dilation (aortic aneurysm)
leads to risk of rupturing

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24
Q

what happens if the coronary artery is affected by atheroma

A

narrowing of the artery lumen-reduced blood flow and ischaemia
thrombus formation over plaque-occlusion of the lumen causing MI

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25
what happens if the iliac and popliteal arteries are affected by atheroma
narrowing of the artery lumen | reduced blood flow leading to ischaemia
26
what happens if the internal carotid arteries are affected by atheroma
emboli travels p the the brain causing ischaemia (if transient) or infraction( TIA/stroke)
27
what is a thrombus
a structured solid mass or plug of blood constituents formed within the heart or blood vessels during life
28
what is thrombosis
the process of thrombus formation-
29
what can thombosis be considered as
the inappropriate activation of the normal haemostatic process
30
where can thrombosis occur
in the CVD anywhere
31
what are the types of thrombus
arterial cardiac venous
32
where do arterial thrombus occur
at sites of endothelial injury or turbulence | usually occlusive lesions
33
when are the common sites of arterial thrombus
coronary arteries cerebral arteries femoral arteries
34
what is a cardiac thrombus also known as
mural thrombi
35
where can cardiac thrombus occur
over areas of endomyocardial injury
36
what else can cardiac thrombus occur with
arrhythmia and cadiomyopathy
37
where can venous thrombus occur
at sites of vascular stasis- in the veins of the lower limbs(DVT)
38
what can be the outcomes of thrombus formation if the patient survives the immediate effects of occlusion
are propagation embolism dissolution-broken down organisation/recanalisation- organise or reattach
39
what are some hypercoagulable conditions
primary( genetic | secondary environmental
40
what are some primary hypercoagulable conditions
protein C or S deficiency antithrombin III factor V mutations prothrombin mutation
41
what are some secondary hypercoagulable decisions
stasis- prolonged bed rest smoking oral contraceptives
42
why can antithrombin III deficiency occur if it is secondary
liver damage
43
what does protein c do
vitamin K dependant glycoprotein inactivates factor Va and VIIIa deficiency increases the risk of clotting
44
describe protein S
vitamin K dependant glycoprotein cofactors works with C helps to inactivate V and VIIIa
45
describe antithrombin III
glycoprotein produced in the liver AKA antithrombin can inherit deficiency can acquire deficiency- due to liver failure
46
what does antithrombin activate
``` factor 9 factor 10 factor 11 12 2 7 ```
47
what are factor V mutations also known as
leiden disease
48
how can oral contraceptive increase the risk of atheroscleorosis
increase in circulating fibrogen
49
how do we clinically prevent thrombosis
aspirin heparin warfarin thrombolysis
50
how is aspirin used
- used for primary and secondary prevention of CVA and MI, and for treatment of MI
51
how is heparin used to prevent thrombosis
to prevent post op DVT
52
how is warfarin used to prevent thrombosis
prevents thrombi in patients with AF and prosthetic heart valves
53
what are the main drugs used in thrombolysis
streptokinase and tissue-type plasminogen activator (TPA)
54
how do streptokinase and TPA work
body’s natural fibrinolytic system to break down thrombus, and minimise myocardial damage.
55
what are some new therapeutics which can be used
Rivaroxaban/apixaban/betrixaban- oral anticoagulant | clopidogrel- anti platelet
56
what is virchows triad
factors predisposing to thrombosis changes in blood constritiency changes in vessel wall changes in pattern of blood flow
57
what can change blood constituents
OCP risks eg obesity personal history social history
58
what can include changes in vessel wall
atheroma trauma inflammation neoplasia
59
what is an embolus
an abnormal mass of material( gas or solid)which is carried in the bloodstream- impacting a vessel whose calibre is too small to let the embolus through
60
describe pulmonary embolism
Embolus originating from detached piece of thrombus sitting in a deep vein of the leg.- Travels via venous system to the right heart, then out through pulmonary artery.- Lodges in pulmonary arterial tree (location depends on size of embolus
61
describe systemic embolism
Embolus originating from detached piece of mural thrombus, or left heart valvular vegetation.- Travels via aorta into systemic arterial circulation.- Can lodge in arteries leading to lower limbs, brain, kidneys or gut.
62
what is a paradoxical embolism
Embolism that originates in systemic veins and enters systemic arterial circulation.
63
what is ischaemia
Impaired vascular perfusion of an area of tissue, thus depriving it of vital nutrients, especially oxygen”
64
what is infarction
Death (necrosis) of an area of tissue due to ischaemia
65
what is shock
’is a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function’
66
what are the four types of shock
cardiogenic obstructive hypovolaemic distributive
67
what is the patheay for shock
inadequate perfusion cell hypoxia energy deficit lactic acid production
68
what are the symptoms of cardiogenic shock
Distended jugular veins due to increased venous pressure Weak or absent pulse Arrhythmia (most frequently tachycardia) Reduced blood pressure
69
what are the symptoms of obstructive shock
Cardiac Tamponade Pulmonary Embolism Aortic Stenosis
70
what are the symptoms of hypovolaemic shock
``` Rapid, weak thready pulse Tachycardia Cool, clammy skin – vasoconstriction Hypothermia Thirst and xerostomia Cold, mottled skin ```
71
symptoms of distributive shock
SIRS (Systemic Inflammatory Response Syndrome) – High resp rate, body temp >36 deg celsius, tachycardia and WBC count between 4000-12000
72
what is the treatment of shock
ABCDE oxygen and bolus of fluid- saline and RBC later vasopressors if hypotension not improved with fluids
73
what is a cardiac tamponade
fluid around the pericardium- heart cannot contract as well cus of fluid