Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

T IoD cellular pathology > cardiovascular pathology I > Flashcards

cardiovascular pathology I Flashcards

1
Q

what is haemostasis?

A

A physiological process for form a solid plug at the site of haemmorhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does haemostasis happen?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the fibrinolytic system there to ensure?

A

That the haemostatic plug doesn’t become too large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does fibrinolysis form?

A

Plasmin which breaks down fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In fibrinolysis what activates the conversion of plasminogen to plasmin?

A

Tissue plasminogen activator

urokinase like plasminogen activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is thrombosis?

A

Inappropriate activation of haemostasis which overwhelms the fibrinolytic system leading to formation of a thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a thrombus made up of, compared to a clot?

A

Thrombus: red blood cells, fibrin, platelets
Clot: Red blood cells and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where does a thrombus form compared to a clot?

A

A thrombus forms in the cardiovascular system where as a clot forms outside of the cardiovascular system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the three groups that make up virchows triad?

A

Endothelial injury
Abnormal blood flow
Hypercoagubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are examples of endothelial injury in virchows triad?

A

Atherosclerosis
vasculitis
direct trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are examples of abnormal blood flow in virchows triad?

A

Turbulence: atherosclerosis, artificial heart valves

stasis: post op, congestive cardiac failure, immobility, pelvic obstruction, aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are examples of hypercoagubility in virchows triad?

A

erythrocytosis
thrombocytosis
hereditary coagulation defects (factor V leiden, protein C/S Deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the most important factors of the virchows triad in arteries?

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the most important factors for thrombus formation in veins?

A

Stasis

hypercoagubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is ischaemia?

A

tissue dysfunction due to interference with blood flow to a tissue. REVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is infarction?

A

tissue necrosis due to interference with blood flow to a tissue. IRREVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is an embolism?

A

occlusion of a vessel by undissolved material that is transported in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are types of emboli?

A 
Fat/bone marrow (due to trauma to long bones)
-Air
amniotic fluid 
tumour
septic emboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is atherosclerosis?

A

A chronic inflammatory process affecting the intima of arteries. it is characterised by formation of lipid plaques in the wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are modifiable risk factors of atherosclerosis?

A

smoking
hypertension
D.M
dyslipidaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what do damaged epithelial cells produc that contributes towards atherosclerosis?

A

adhesion molecules and cytokines which attract inflammatory cells and prothrombotic molecules
VCAM binds monocytes and t cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the effects of macrophages in atherosclerosis formation?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is a ‘fatty streak?’

A

Collections of lipid laden macrophages sitting in the intimal layer which can be visible as yellow streaks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is an atherosclerotic plaque?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the three hallmarks of chronic inflammation?
- persistant injury - on going inflammation - repair with scarring
26
what determines atherosclerotic plaque stability?
the balance between the number of smooth muscle cells and the number of inflammatory cells in the fibrous cap
27
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
28
what are smooth muscle cells protective to atherosclerotic plaque stability?
they produce the fibrous cap and produce tissue inhibitors of MMP's
29
How can atherosclerosis contribute towards stable angina?
Gradual enlargement of the plaque leads to luminal stenosis, due to poiseuilles law this affects flow
30
what can atherosclerosis contribute towards MI?
Sudden rupture of a vulnerable plaque can lead to occlusion
31
what is meant by ischaemic heart disease?
Covers diseases that are caused by coronary artery atherosclerosis
32
what is the presentation of stable angina?
A predictable cardiac pain Precipitated by exertion lasting 1-2 minutes relieved by GTN
33
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.
34
what are acute coronary syndromes?
clinical conditions caused by severe reduction in myocardial perfusion leading to ischaemia.
35
what troponin levels tend to be used clinically?
T and I
36
If there is no ST elevation and negative troponins what is the responsible acute coronary syndrome?
unstable angina
37
if there is no ST elevation and positive troponin what acute coronary syndrome is responsible?
NSTEMI
38
what is wrong with the artery in NSTEMI/ unstable angina?
It's PARTIALLY occluded
39
What is wrong with the artery in a STEMI?
it is totally occluded
40
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
41
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
42
how does the myocardium change within 12 hours of MI?
no naked eye changes by microscopic myocyte necrosis
43
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
44
how does the myocardium change within 3-10 days of MI?
hyperemic border to the naked eye | organisation of the infarct with granulation tissue
45
what ECG leads are for inferior MI?
II,III,AvF
46
what ECG leads are for anterior MI?
V1-V4
47
what ECG leads are for a lateral MI?
I,AVL,V5-6
48
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
49
If after MI there is myocardium rupture what happens if it's rupture of the free wall of the ventricle?
haemipericardium and cardiac tamponade
50
If after MI there is myocardium rupture what happens if it's rupture of the papillary muscle of the mitral valve?
acute mitral regurgitation.
51
what are long term complications of an MI?
- recurrent MI - chronic congestive ehart failure - dresslers syndrome - ventricular aneurysm formaiton
52
what is the most common type of stroke?
Ischaemic
53
what causes an ischaemic stroke?
sudden occlusion of a cerebral artery leading to sudden reduction in blood flow
54
what is the most common artery for a plaque to arise from that causes an ischameic stroke?
internal carotid artery
55
what is a saccular aneurysm?
spherical shape bulging out the side of the vessel
56
what is a fusiform aneurysm?
spindle shaped involving all the circumferece of the vessel
57
how is an aortic aneurysm defined?
a diameter of over 3cm
58
who is invited for AA screening?
Men aged 65
59
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
60
what are D dimers?
fibrin degredation produces and are raised in PE
61
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
62
what is a common cause of a slow rising pulse?
Aortic Stenosis

T IoD cellular pathology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions