IOD CVS Pathology I Flashcards
Haemostasis?
Haemostasis occurs when there is damage to a blood vessel
it involves the formation of a solid plug from the constituents of blood
it stops loss of blood from the circulation at the site of injury
it is physiological (ie. it’s a good thing)
What does haemostasis depend on?
close interactions between the vessel wall, platelets and the
coagulation cascade:
platelets stick to the wall
turbulent flow stimulates a chemical reaction in platelets to activate them
endothelial cells in the wall release cytokines and stimulate contraction
Process of haemostasis?
Endothelial injury leads to adhesion and aggregation of platelets
formation of a loose (primary) platelet plug
At the same time, exposure of tissue factor initiates the coagulation cascade formation of insoluble fibrin
Fibrin stabilises the loose platelet plug to form a stable (secondary) platelet plug
why is a cascade good?
exponential amplification of products
better control
fibrinolysis?
The haemostatic plug is then broken down by activation of the fibrinolytic system
Fibrinolysis is activated by the same injury that initiates haemostasis
Plasminogen is converted to plasmin. Plasmin degrades insoluble fibrin to soluble products
more anti-clotting factors than pro-clotting factors
thrombosis?
Thrombosis occurs when there is inappropriate activation of haemostasis:
platelets and the coagulation system interact with the vessel wall to form a solid plug (=thrombus) in the blood vessel
the process overwhelms the capacity of the fibrinolytic system and coagulation inhibitors
thrombus?
A thrombus is made up of the same components as a haemostatic plug ie. platelets, fibrin and red blood cells but is pathological
thrombus vs clot?
t-Composed of red blood cells, fibrin and platelets, flows in CVS in flowing blood
c-composed of rbcs a and fibrin no platelets-outside cvs in stationary blood
Virchows triad?
Endothelial Injury Atherosclerosis Vasculitis
Direct trauma
Abnormal blood flow Turbulence
Stasis
Hypercoagulability Blood cells (too many)
Alterations in coagulation factors
most important risk factor in arterial thrombosis?
AS or endothelial injury
most important risk factor in venous thrombosis?
stasis and hypercoagulability
causes of thrombi?
smoking malignancy-paraneoplastic eg small cell lung carcinoma or SCC protein c and s-vit K dep Factor V leiden-mutation OCP Antiphospholipid syndrome myeloproliferative Haemoglobinuria
complications of thrombi?
partial occlusion
complete occlusion
embolism distant site as undissolved material
which materials can occlude a vessel?
TE fat DIC air macro bolus/micro amniotic fluid tumour -LA myoxoma infective endocarditis cholesterol foreign material
ischaemia?
tissue dysfunction due to interference with blood flow (supply or drainage) to a tissue. It is reversible
infarction?
tissue death (necrosis) due to interference with blood flow (supply or drainage) to a tissue. It is irreversible
necrosis?
cell death due to a pathological process
TE occlude where?
pulmonary artery
TE in atrial/left side of feart occludes…?
systemic artery
AS?
chronic inflammatory process centred on the intima (endothelium) of large and medium sized arteries
AS risk factors?
It is initiated by endothelial injury which is caused by well known risk factors including:
smoking
hypertension
diabetes
dyslipidaemia (abnormal lipoprotein levels ie. high ratio of LDL:HDL)/hypercholaemia LDL
FH
male
complications of AS?
Gradual enlargement of a stable plaque leading to luminal stenosis
Sudden disruption of a vulnerable plaque followed by thrombosis in the vessel lumen
Aneurysm formation
-rupture or TE
stable angina, ACS, TIA, CVA, Bowel ischaemia, renal artery stenosis and PVD
what is plaque stability determined by?
smooth muscle cells (produce fibrous cap that stabilises the plaque)
inflammatory cells (digest the fibrous cap and kill smooth muscle cells
destabilise the plaque)
stable vs unstable plaques?
Stable plaques have a thick fibrous cap that is resistant to rupture. These stable lesions grow slowly in size over decades resulting in gradual stenosis
Unstable ‘vulnerable’ plaques contain more inflammatory cells and have a thinner fibrous cap that is prone to acute rupture
definition stable angina?
An imbalance between O2 supply and O2 demand in the myocardium:
Exertion → ↑O2 demand by myocardium
→ mismatch O2 supply/demand
→ myocardial ischaemia
→ cardiac-type pain
Clinically:
– predictable cardiac-type pain (precipitated by exertion), relieved by rest
Cause: stenosis due to a stable plaque in a coronary artery
ECG findings in stable angina?
ST elevation myocardial infarction (STEMI)
ST elevation in leads II, III and aVF
[there is also reciprocal ST depression in V1-3, I and aVL
ACS definition?
Spectrum of clinical conditions when Sudden plaque disruption and thrombosis occurs
Partial or complete occlusion of the coronary artery at the site of disruption and marked spasm of the vessel
Unstable angina and NSTEMI?
occur when there is partial occlusion of a coronary artery:
This results in ischaemia or infarction of the myocardium supplied by the affected coronary artery
Unstable angina and NSTEMI differ mainly in the severity of myocardial ischaemia:
– in NSTEMI the ischaemia is severe enough to result in release of cardiac troponins into blood
How many ACS are each?
STEMI-40%
NSTEMI-60%
STEMI?
occurs when there is complete occlusion of a coronary artery
ST elevation and raised troponin (greater than in NSTEMI)
There is transmural infarction of the myocardium supplied by the affected coronary artery
Link to anatomy?
RCA-RA, RV pacemaker inferior LV/MI ECG leads II, III, AVF LCA-Lateral LV/MI ECG leads I, aVL, V5-6 LAD-anterior LV/MI ECG leads V1-4
body’s response to MI?
acute inflammation to myocyte necrosis
timeline-0-12 hrs?
myocyte necrosis
timeline-12-72 hrs
acute inflammatory response-neutrophils invade tissue
granulation tissue rim and solution of loose fibrous tissue and capillaries
timeline 3-10 days?
hyperaemia, yellow to white fibrous scar as granulation tissue replaces cells
timeline up to 6 wks?
scar formation due to collagen deposition-white scar
Vfib?
It presents as cardiac arrest
It is probably related to K+ released from necrotic myocytes which induce arrhythmias in the hyper-excitable tissue around the infarct
Other arrhythmias may also occur as complications of MI (eg. bradycardia, ventricular tachycardia, supraventricular tachycardia)
Arrhythmias are more commonly seen in inferior MIs.
inferior MI’s lead to arrhythmias as?
The right coronary artery supplies the inferior LV and the pacemaker
can lead to complete heart block
what can rupture in an MI?
Rupture of the free wall of the ventricle → haemopericardium
→ cardiac tamponade
what else can rupture in an MI?
IV septum-ventricular septal defect
what muscle ruptures in an MI?
Rupture of the papillary muscle of the valve causing acute mitral regurgitation
mural thrombus?
thrombus inside ventricular wall silent MI cause endothelial injury stasis embolisation
pericarditis?
A transmural infarct extends to involve the pericardium, inciting an inflammatory response
acute chest pain and STE and pleural rub
ventricular aneurysms?
Complications include thromboembolism, arrhythmias and heart failure
NB. Ventricular aneurysms rarely rupture because they are composed of tough fibrous tissue
Dressler’s syndrome?
Autoimmune pericarditis 2-10 months after full thickness MI
Risk of PE and pleural effusion
shoulder hands syndrome?
left arm fatigue and atrophy due to lack of optimal loading
spectrum of IHD?
see ppt
How does chronic IHD lead to HF?
low grade chronic ischaemia progressive fine diffuse myocardial fibrosis reduced contractile function decompensation CHF onset
PE?
always due to transportation of thrombus in the bloodstream which then impacts in a pulmonary artery
The thrombus may originate in the: leg (80%) – deep vein thrombosis pelvis arm right ventricle
Which system estimates a PE?
Two-level PE Wells score
see ppt
signs of PE on ECG?
ECG sinus tachy, af, right bundle brunch block, s1 q3 t3
ischaemic stroke pathophys?
Most commonly, an atherosclerotic plaque in an internal carotid artery ruptures and thrombus forms on the surface of the plaque
Part of the thrombus embolises and occludes one of the cerebral arteries resulting in a stroke
AAA?
AS is single most important risk factor in developing an AAA
Complications of AAA?
rupture
Thrombus formation
TE
