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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

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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

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3
Q

what is the fibrinolytic system there to ensure?

A

That the haemostatic plug doesn’t become too large

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4
Q

what does fibrinolysis form?

A

Plasmin which breaks down fibrin

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5
Q

In fibrinolysis what activates the conversion of plasminogen to plasmin?

A

Tissue plasminogen activator

urokinase like plasminogen activator

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6
Q

what is thrombosis?

A

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

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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

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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.

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9
Q

what are the three groups that make up virchows triad?

A

Endothelial injury
Abnormal blood flow
Hypercoagubility

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10
Q

what are examples of endothelial injury in virchows triad?

A

Atherosclerosis
vasculitis
direct trauma

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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

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12
Q

what are examples of hypercoagubility in virchows triad?

A

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

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13
Q

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

A

Atherosclerosis

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14
Q

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

A

Stasis

hypercoagubility

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15
Q

what is ischaemia?

A

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

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16
Q

what is infarction?

A

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

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17
Q

what is an embolism?

A

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

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18
Q

what are types of emboli?

A 
Fat/bone marrow (due to trauma to long bones)
-Air
amniotic fluid 
tumour
septic emboli
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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.

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20
Q

what are modifiable risk factors of atherosclerosis?

A

smoking
hypertension
D.M
dyslipidaemia

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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

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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
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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

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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

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25
Q

what are the three hallmarks of chronic inflammation?

A
  • persistant injury
  • on going inflammation
  • repair with scarring
26
Q

what determines atherosclerotic plaque stability?

A

the balance between the number of smooth muscle cells and the number of inflammatory cells in the fibrous cap

27
Q

how do inflammatory cells in the fibrous cap destabilise the atherosclerotic plaque?

A

They produce MMP’s which digest the fibrous cap and cause smooth muscle cells to undergo apoptosis

28
Q

what are smooth muscle cells protective to atherosclerotic plaque stability?

A

they produce the fibrous cap and produce tissue inhibitors of MMP’s

29
Q

How can atherosclerosis contribute towards stable angina?

A

Gradual enlargement of the plaque leads to luminal stenosis, due to poiseuilles law this affects flow

30
Q

what can atherosclerosis contribute towards MI?

A

Sudden rupture of a vulnerable plaque can lead to occlusion

31
Q

what is meant by ischaemic heart disease?

A

Covers diseases that are caused by coronary artery atherosclerosis

32
Q

what is the presentation of stable angina?

A

A predictable cardiac pain
Precipitated by exertion lasting 1-2 minutes
relieved by GTN

33
Q

other than atherosclerosis what other diseases can cause stable angina/

A

Aortic stenosis as it leads to left ventricular hypertrophy and demand can’t be met.

34
Q

what are acute coronary syndromes?

A

clinical conditions caused by severe reduction in myocardial perfusion leading to ischaemia.

35
Q

what troponin levels tend to be used clinically?

A

T and I

36
Q

If there is no ST elevation and negative troponins what is the responsible acute coronary syndrome?

A

unstable angina

37
Q

if there is no ST elevation and positive troponin what acute coronary syndrome is responsible?

A

NSTEMI

38
Q

what is wrong with the artery in NSTEMI/ unstable angina?

A

It’s PARTIALLY occluded

39
Q

What is wrong with the artery in a STEMI?

A

it is totally occluded

40
Q

what is the preferred management for STEMI?

A
  • 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
Q

what is the management for NSTEMI/ unstable angina?

A

patients at high risk are offered coronary angiogrpaphy with PCI within 96 hours
- stable are offered angiography

42
Q

how does the myocardium change within 12 hours of MI?

A

no naked eye changes by microscopic myocyte necrosis

43
Q

how does the myocardium change within 12-24 hours of MI?

A

Pale to the naked eye

Necrosis starts an acute inflammatory response s neutrophils infiltrate cardiac muscle

44
Q

how does the myocardium change within 3-10 days of MI?

A

hyperemic border to the naked eye

organisation of the infarct with granulation tissue

45
Q

what ECG leads are for inferior MI?

A

II,III,AvF

46
Q

what ECG leads are for anterior MI?

A

V1-V4

47
Q

what ECG leads are for a lateral MI?

A

I,AVL,V5-6

48
Q

what are short term complications of MI?

A

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
Q

If after MI there is myocardium rupture what happens if it’s rupture of the free wall of the ventricle?

A

haemipericardium and cardiac tamponade

50
Q

If after MI there is myocardium rupture what happens if it’s rupture of the papillary muscle of the mitral valve?

A

acute mitral regurgitation.

51
Q

what are long term complications of an MI?

A
  • recurrent MI
  • chronic congestive ehart failure
  • dresslers syndrome
  • ventricular aneurysm formaiton
52
Q

what is the most common type of stroke?

A

Ischaemic

53
Q

what causes an ischaemic stroke?

A

sudden occlusion of a cerebral artery leading to sudden reduction in blood flow

54
Q

what is the most common artery for a plaque to arise from that causes an ischameic stroke?

A

internal carotid artery

55
Q

what is a saccular aneurysm?

A

spherical shape bulging out the side of the vessel

56
Q

what is a fusiform aneurysm?

A

spindle shaped involving all the circumferece of the vessel

57
Q

how is an aortic aneurysm defined?

A

a diameter of over 3cm

58
Q

who is invited for AA screening?

A

Men aged 65

59
Q

what is the wells criteria?

A

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
Q

what are D dimers?

A

fibrin degredation produces and are raised in PE

61
Q

when would you do a D dimer?

A
  • clinical suspicion of a PE and wells score under 2

- if wells is above 4 go straight to CTPA

62
Q

what is a common cause of a slow rising pulse?

A

Aortic Stenosis

T IoD cellular pathology (10 decks)

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