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IOD CVS Pathology I Flashcards

1
Q

Haemostasis?

A

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)

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2
Q

What does haemostasis depend on?

A

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

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3
Q

Process of haemostasis?

A

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

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4
Q

why is a cascade good?

A

exponential amplification of products

better control

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5
Q

fibrinolysis?

A

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

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6
Q

thrombosis?

A

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

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7
Q

thrombus?

A

A thrombus is made up of the same components as a haemostatic plug ie. platelets, fibrin and red blood cells but is pathological

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8
Q

thrombus vs clot?

A

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

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9
Q

Virchows triad?

A

Endothelial Injury Atherosclerosis Vasculitis
Direct trauma
Abnormal blood flow Turbulence
Stasis
Hypercoagulability Blood cells (too many)
Alterations in coagulation factors

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10
Q

most important risk factor in arterial thrombosis?

A

AS or endothelial injury

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11
Q

most important risk factor in venous thrombosis?

A

stasis and hypercoagulability

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12
Q

causes of thrombi?

A 
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
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13
Q

complications of thrombi?

A

partial occlusion
complete occlusion
embolism distant site as undissolved material

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14
Q

which materials can occlude a vessel?

A 
TE
fat
DIC
air macro bolus/micro
amniotic fluid
tumour -LA myoxoma
infective endocarditis
cholesterol
foreign material
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15
Q

ischaemia?

A

tissue dysfunction due to interference with blood flow (supply or drainage) to a tissue. It is reversible

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16
Q

infarction?

A 
tissue death (necrosis) due to interference with blood flow (supply or drainage)
to a tissue. It is irreversible
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17
Q

necrosis?

A

cell death due to a pathological process

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18
Q

TE occlude where?

A

pulmonary artery

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19
Q

TE in atrial/left side of feart occludes…?

A

systemic artery

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20
Q

AS?

A

chronic inflammatory process centred on the intima (endothelium) of large and medium sized arteries

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21
Q

AS risk factors?

A

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

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22
Q

complications of AS?

A

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

23
Q

what is plaque stability determined by?

A

smooth muscle cells (produce fibrous cap that stabilises the plaque)
inflammatory cells (digest the fibrous cap and kill smooth muscle cells
 destabilise the plaque)

24
Q

stable vs unstable plaques?

A

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

25
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
26
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
27
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
28
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
29
How many ACS are each?
STEMI-40% | NSTEMI-60%
30
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
31
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 ```
32
body's response to MI?
acute inflammation to myocyte necrosis
33
timeline-0-12 hrs?
myocyte necrosis
34
timeline-12-72 hrs
acute inflammatory response-neutrophils invade tissue | granulation tissue rim and solution of loose fibrous tissue and capillaries
35
timeline 3-10 days?
hyperaemia, yellow to white fibrous scar as granulation tissue replaces cells
36
timeline up to 6 wks?
scar formation due to collagen deposition-white scar
37
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.
38
inferior MI's lead to arrhythmias as?
The right coronary artery supplies the inferior LV and the pacemaker can lead to complete heart block
39
what can rupture in an MI?
Rupture of the free wall of the ventricle → haemopericardium | → cardiac tamponade
40
what else can rupture in an MI?
IV septum-ventricular septal defect
41
what muscle ruptures in an MI?
Rupture of the papillary muscle of the valve causing acute mitral regurgitation
42
mural thrombus?
``` thrombus inside ventricular wall silent MI cause endothelial injury stasis embolisation ```
43
pericarditis?
A transmural infarct extends to involve the pericardium, inciting an inflammatory response acute chest pain and STE and pleural rub
44
ventricular aneurysms?
Complications include thromboembolism, arrhythmias and heart failure NB. Ventricular aneurysms rarely rupture because they are composed of tough fibrous tissue
45
Dressler's syndrome?
Autoimmune pericarditis 2-10 months after full thickness MI | Risk of PE and pleural effusion
46
shoulder hands syndrome?
left arm fatigue and atrophy due to lack of optimal loading
47
spectrum of IHD?
see ppt
48
How does chronic IHD lead to HF?
``` low grade chronic ischaemia progressive fine diffuse myocardial fibrosis reduced contractile function decompensation CHF onset ```
49
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 ```
50
Which system estimates a PE?
Two-level PE Wells score | see ppt
51
signs of PE on ECG?
ECG sinus tachy, af, right bundle brunch block, s1 q3 t3
52
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
53
AAA?
AS is single most important risk factor in developing an AAA
54
Complications of AAA?
rupture Thrombus formation TE

CVS (30 decks)

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