cardiovascular pathology I Flashcards
what is haemostasis?
A physiological process for form a solid plug at the site of haemmorhage
how does haemostasis happen?
Endothelial injury meaning adhesion of platelets to collagen by VWF –> red blood cells become meshed in with the platelets –> formation of a loose –> coagulation cascade–> solid plug
what is the fibrinolytic system there to ensure?
That the haemostatic plug doesn’t become too large
what does fibrinolysis form?
Plasmin which breaks down fibrin
In fibrinolysis what activates the conversion of plasminogen to plasmin?
Tissue plasminogen activator
urokinase like plasminogen activator
what is thrombosis?
Inappropriate activation of haemostasis which overwhelms the fibrinolytic system leading to formation of a thrombus
What is a thrombus made up of, compared to a clot?
Thrombus: red blood cells, fibrin, platelets
Clot: Red blood cells and fibrin
where does a thrombus form compared to a clot?
A thrombus forms in the cardiovascular system where as a clot forms outside of the cardiovascular system.
what are the three groups that make up virchows triad?
Endothelial injury
Abnormal blood flow
Hypercoagubility
what are examples of endothelial injury in virchows triad?
Atherosclerosis
vasculitis
direct trauma
what are examples of abnormal blood flow in virchows triad?
Turbulence: atherosclerosis, artificial heart valves
stasis: post op, congestive cardiac failure, immobility, pelvic obstruction, aneurysms
what are examples of hypercoagubility in virchows triad?
erythrocytosis
thrombocytosis
hereditary coagulation defects (factor V leiden, protein C/S Deficiency)
what are the most important factors of the virchows triad in arteries?
Atherosclerosis
what are the most important factors for thrombus formation in veins?
Stasis
hypercoagubility
what is ischaemia?
tissue dysfunction due to interference with blood flow to a tissue. REVERSIBLE
what is infarction?
tissue necrosis due to interference with blood flow to a tissue. IRREVERSIBLE
what is an embolism?
occlusion of a vessel by undissolved material that is transported in the blood
what are types of emboli?
Fat/bone marrow (due to trauma to long bones) -Air amniotic fluid tumour septic emboli
what is atherosclerosis?
A chronic inflammatory process affecting the intima of arteries. it is characterised by formation of lipid plaques in the wall.
what are modifiable risk factors of atherosclerosis?
smoking
hypertension
D.M
dyslipidaemia
what do damaged epithelial cells produc that contributes towards atherosclerosis?
adhesion molecules and cytokines which attract inflammatory cells and prothrombotic molecules
VCAM binds monocytes and t cells
what are the effects of macrophages in atherosclerosis formation?
- they produce free radicals that drive LDL oxidation
- they eat oxidised LDL and cholesterol to form foam cells
- the foam cells produce growth factors that promote migration of smooth muscle from the media to the intima
what is a ‘fatty streak?’
Collections of lipid laden macrophages sitting in the intimal layer which can be visible as yellow streaks
what is an atherosclerotic plaque?
A core of lipid debris forms as the foamy macrophages die and the lipid is released.
Smooth muscle cells proliferate and secrete collagen and form a fibrous cap
what are the three hallmarks of chronic inflammation?
- persistant injury
- on going inflammation
- repair with scarring
what determines atherosclerotic plaque stability?
the balance between the number of smooth muscle cells and the number of inflammatory cells in the fibrous cap
how do inflammatory cells in the fibrous cap destabilise the atherosclerotic plaque?
They produce MMP’s which digest the fibrous cap and cause smooth muscle cells to undergo apoptosis
what are smooth muscle cells protective to atherosclerotic plaque stability?
they produce the fibrous cap and produce tissue inhibitors of MMP’s
How can atherosclerosis contribute towards stable angina?
Gradual enlargement of the plaque leads to luminal stenosis, due to poiseuilles law this affects flow
what can atherosclerosis contribute towards MI?
Sudden rupture of a vulnerable plaque can lead to occlusion
what is meant by ischaemic heart disease?
Covers diseases that are caused by coronary artery atherosclerosis
what is the presentation of stable angina?
A predictable cardiac pain
Precipitated by exertion lasting 1-2 minutes
relieved by GTN
other than atherosclerosis what other diseases can cause stable angina/
Aortic stenosis as it leads to left ventricular hypertrophy and demand can’t be met.
what are acute coronary syndromes?
clinical conditions caused by severe reduction in myocardial perfusion leading to ischaemia.
what troponin levels tend to be used clinically?
T and I
If there is no ST elevation and negative troponins what is the responsible acute coronary syndrome?
unstable angina
if there is no ST elevation and positive troponin what acute coronary syndrome is responsible?
NSTEMI
what is wrong with the artery in NSTEMI/ unstable angina?
It’s PARTIALLY occluded
What is wrong with the artery in a STEMI?
it is totally occluded
what is the preferred management for STEMI?
- patients assessed for IMMEDIATE coronary repurfusion
- coronary angiography with follow on primary percutaneous intervention
patient should present within 12 hours and PCI within 120 minutes if not alteplase/reteplase offered
what is the management for NSTEMI/ unstable angina?
patients at high risk are offered coronary angiogrpaphy with PCI within 96 hours
- stable are offered angiography
how does the myocardium change within 12 hours of MI?
no naked eye changes by microscopic myocyte necrosis
how does the myocardium change within 12-24 hours of MI?
Pale to the naked eye
Necrosis starts an acute inflammatory response s neutrophils infiltrate cardiac muscle
how does the myocardium change within 3-10 days of MI?
hyperemic border to the naked eye
organisation of the infarct with granulation tissue
what ECG leads are for inferior MI?
II,III,AvF
what ECG leads are for anterior MI?
V1-V4
what ECG leads are for a lateral MI?
I,AVL,V5-6
what are short term complications of MI?
Ventricular fibrillation –> sudden death due to the potassium released from necrotic myocytes
arrythmia
Acute cardiac failure as the infarcted myocytes can’t contract properly
myocardium rupture
pericarditis
A mural thrombus
If after MI there is myocardium rupture what happens if it’s rupture of the free wall of the ventricle?
haemipericardium and cardiac tamponade
If after MI there is myocardium rupture what happens if it’s rupture of the papillary muscle of the mitral valve?
acute mitral regurgitation.
what are long term complications of an MI?
- recurrent MI
- chronic congestive ehart failure
- dresslers syndrome
- ventricular aneurysm formaiton
what is the most common type of stroke?
Ischaemic
what causes an ischaemic stroke?
sudden occlusion of a cerebral artery leading to sudden reduction in blood flow
what is the most common artery for a plaque to arise from that causes an ischameic stroke?
internal carotid artery
what is a saccular aneurysm?
spherical shape bulging out the side of the vessel
what is a fusiform aneurysm?
spindle shaped involving all the circumferece of the vessel
how is an aortic aneurysm defined?
a diameter of over 3cm
who is invited for AA screening?
Men aged 65
what is the wells criteria?
This is used to assess the likelihood of PE.
- clinical symptoms of DVT
- Heart rate over 100bpm
- previous DVT/PE
- haemoptysis
- immobilisation/surgery in the last 4 week
- malignant
what are D dimers?
fibrin degredation produces and are raised in PE
when would you do a D dimer?
- clinical suspicion of a PE and wells score under 2
- if wells is above 4 go straight to CTPA
what is a common cause of a slow rising pulse?
Aortic Stenosis
