Atherosclerosis thrombosis and embolism Flashcards
we will cover atherosclerosis thrombosis and emboli types of risk factors development treatment prevention ischaemia and infarction shock
how many people die each year from a hospital acquired venousthrombo embolism
32000
describe the physiology of blood vessels and endothelial cells
inner layer: intima
middle media
outer- adventitia
what is the difference between the media in a vein and an artery
the media in the artery is much bigger diameter
what is the origin of endothelial cells
mesodermal origin
what are endothelial cells found
interior surface of blood vessels and the lymphatics and on the inside of the heart( called the endocardium)
what are endothelial cells called inside the heart
endocardium
what is the function of the endothelial cells
semi selective barrier function- allows WBC to move out to the area of infection (diapedesis)
- angiogenesis
- mediator of coagulation
- blood pressure control
- fluid filtration
what happens with prolonged inflammation to the endothelial cells
increased permeability and tissue swelling
what clotting factors do endothelial cells mediate
von willibrands factor- stabilises factor VIII which binds to collagen linking platelets
heparan sulphate- inactivates clotting cascade
what does heparan sulphate control
inactivates clotting cascade
which diseases is endothelial cell dysfunction
many diseases
septic shock
hypertension
behcets
how else can endothelial cell dysfunction arise
tobacco and air pollution
trans fat consumption
how can endothelial cell dysfunction improve
smoking cessation
weight loss
improved diet
exercise
what is a atheroma
is an accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries
what is atherosclerosis
the thickening and hardening of arterial walls as a consequence of atheroma
why do atheromas form
due to chronic endothelial cell damage- in the arteries as BP is higher
how does an atheroma develop 11 steps
- 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
what are the risk factors for atheroma
high LDL/low HDL hypertension diabetes sedentary lifestyle obesity smoking
what are the two forms of prevention for the formation of atherosclerosis
primary- risk factor modification
secondary- includes regulation medications such as aspirin and the prevention of the recurrence of events
when do early atheromas start forming
in your early 20s-30s
progressive
which medications can be used to stabilise the plaques and prevent rupture
statins
what medication can be used if the atheroma was to rupture
antithrombotic agents
which sites can be affected
aorta-
coronary artery
iliac and popliteal arteries
internal carotid arteries
iwhat happens if the aorta is affected by atheroma
weakening of the aorta can cause aortic aneurysm and then risk of rupturing
what happens if the coronary artery is affected by atheroma
narrowing of the artery lumen-reduced blood flow and ischaemia
thrombus formation over plaque-occlusion of the lumen causing MI
what happens if the iliac and popliteal arteries are affected by atheroma
narrowing of the artery lumen
reduced blood flow leading to ischaemia
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)
what is a thrombus
a structured solid mass or plug of blood constituents formed within the heart or blood vessels during life
what is thrombosis
the process of thrombus formation-
what can thombosis be considered as
the inappropriate activation of the normal haemostatic process
where can thrombosis occur
in the CVD anywhere
what are the types of thrombus
arterial
cardiac
venous
where do arterial thrombus occur
at sites of endothelial injury or turbulence
usually occlusive lesions
when are the common sites of arterial thrombus
coronary arteries
cerebral arteries
femoral arteries
what is a cardiac thrombus also known as
mural thrombi
where can cardiac thrombus occur
over areas of endomyocardial injury
what else can cardiac thrombus occur with
arrhythmia and cadiomyopathy
where can venous thrombus occur
at sites of vascular stasis- in the veins of the lower limbs(DVT)
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
what are some hypercoagulable conditions
primary( genetic
secondary environmental
what are some primary hypercoagulable conditions
protein C or S deficiency
antithrombin III
factor V mutations
prothrombin mutation
what are some secondary hypercoagulable decisions
stasis- prolonged bed rest
smoking
oral contraceptives
why can antithrombin III deficiency occur if it is secondary
liver damage
what does protein c do
vitamin K dependant glycoprotein
inactivates factor Va and VIIIa
deficiency increases the risk of clotting
describe protein S
vitamin K dependant glycoprotein
cofactors works with C
helps to inactivate V and VIIIa
describe antithrombin III
glycoprotein produced in the liver
AKA antithrombin
can inherit deficiency
can acquire deficiency- due to liver failure
what does antithrombin activate
factor 9 factor 10 factor 11 12 2 7
what are factor V mutations also known as
leiden disease
how can oral contraceptive increase the risk of atheroscleorosis
increase in circulating fibrogen
how do we clinically prevent thrombosis
aspirin
heparin
warfarin
thrombolysis
how is aspirin used
- used for primary and secondary prevention of CVA and MI, and for treatment of MI
how is heparin used to prevent thrombosis
to prevent post op DVT
how is warfarin used to prevent thrombosis
prevents thrombi in patients with AF and prosthetic heart valves
what are the main drugs used in thrombolysis
streptokinase and tissue-type plasminogen activator (TPA)
how do streptokinase and TPA work
body’s natural fibrinolytic system to break down thrombus, and minimise myocardial damage.
what are some new therapeutics which can be used
Rivaroxaban/apixaban/betrixaban- oral anticoagulant
clopidogrel- anti platelet
what is virchows triad
factors predisposing to thrombosis
changes in blood constritiency
changes in vessel wall
changes in pattern of blood flow
what can change blood constituents
OCP
risks eg obesity
personal history
social history
what can include changes in vessel wall
atheroma
trauma
inflammation
neoplasia
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
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
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.
what is a paradoxical embolism
Embolism that originates in systemic veins and enters systemic arterial circulation.
what is ischaemia
Impaired vascular perfusion of an area of tissue, thus depriving it of vital nutrients, especially oxygen”
what is infarction
Death (necrosis) of an area of tissue due to ischaemia
what is shock
’is a life-threateningmedicalcondition of low bloodperfusionto tissues resulting in cellular injury and inadequate tissue function’
what are the four types of shock
cardiogenic
obstructive
hypovolaemic
distributive
what is the patheay for shock
inadequate perfusion
cell hypoxia
energy deficit
lactic acid production
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
what are the symptoms of obstructive shock
Cardiac Tamponade
Pulmonary Embolism
Aortic Stenosis
what are the symptoms of hypovolaemic shock
Rapid, weak thready pulse Tachycardia Cool, clammy skin – vasoconstriction Hypothermia Thirst and xerostomia Cold, mottled skin
symptoms of distributive shock
SIRS (Systemic Inflammatory Response Syndrome) – High resp rate, body temp >36 deg celsius, tachycardia and WBC count between 4000-12000
what is the treatment of shock
ABCDE
oxygen and bolus of fluid- saline and RBC later
vasopressors if hypotension not improved with fluids
what is a cardiac tamponade
fluid around the pericardium- heart cannot contract as well cus of fluid
