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Cardiovascular: pathology > Atheroma, thrombosis and embolism > Flashcards

Atheroma, thrombosis and embolism Flashcards

1
Q

is ischaemia reversible?

A

yes depending on multiple factors including speed of onset, local demand and duration

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2
Q

is infarction reversible

A

no, you get repair by scarring .

In the liver though you may get regeneration

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3
Q

what are the 2 functions of haemostasis?

A

1 – maintain blood in a fluid, clot free state in normal vessels;
2 – induce rapid, localised haemostatic plug at site of vascular injury.

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4
Q

what is thrombosis ?

A

pathological corruption of haemostasis. The formation of a solid or semi-solid mass from the constituents of blood, within the vascular system, during life.

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5
Q

what is the role of platelets?

A

to close small breaches in vessel walls

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6
Q

what are the haemostatic contents of platelet alpha granules

A

adhesion components e.g. fibrinogen, fibronecton, PGDF, anti-heparin. Also vWF and factor V

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7
Q

what are the haemostatic contents of platelet dense granules

A

they are important for aggregation and contain ADP and 5HT

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8
Q

what are the 8 main functions of endothelial cells

A
  1. maintain a permeability barrier
  2. elaborates anticoagulant, antithrombotis, fibrinolytic regulators
  3. elaborates prothrombotic molecules
  4. produces EC matrix
  5. modulates blood flow and vascular reactivity
  6. regulates inflammation and immunity
  7. regulates cell growth
  8. role in LDL oxidation
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9
Q

give some examples of the anticoagulant, antithrombotic, fibrinolytic regulators produced by endothelial cells?

A

Prostacylcin, Thrombomodulin, Heparin-like molecules, Plasminogen activator

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10
Q

give some examples of the prothrombotic molecules produced by endothelial cells?

A

VWF, Tissue Factor, Plasminogen activator inhibitor

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11
Q

how do endothelial cells modulate blood flow and vascular reactivity?

A

by secreting:

  • Vasoconstrictors – endothelin, ACE
  • Vasodilators – NO, prostacylcin
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12
Q

how do endothelial cells Regulates inflammation and immunity?

A

by
IL-1, IL-6, chemokines

Adhesion molecules – VCAM-1, ICAM-1, E-selectin, P-selectin

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13
Q

how do endothelial cells Regulates cell growth?

A

Growth stimulators

Growth inhibitors

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14
Q

name examples of growth stimulators?

A

PDGF, CSF, FGF

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15
Q

name examples of growth inhibitors?

A

heparin, TGF-beta

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16
Q

what are some causes of endothelial injury ?

A 
Hyperlipidaemia
Hypertension
Smoking
Toxins
Vasculitis
Viruses - cytomegalo virus e.g. 
Immune reactions- coagulation cascade, antibody complexes
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17
Q

what effects does stasis and turbulence have? 4 things

A
  1. platelets come into contact with the endothelium
  2. activated clotting factors are not dilutes by the normal rapid flow of blood
  3. inflow of anticoagulant factors is slowed, allowing thrombi to persist
  4. activation of endothelial cells in promoted
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18
Q

what are some examples of situations in which turbulence and stasis are important factors in thrombosis ?? name 4

A
  1. DVT
  2. non -contractile areas of myocardium following an MI
  3. aneurysm
  4. AF
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19
Q

what is hypercoagulability?

A

any alteration in the coagulation pathway which predisposes to thrombosis.

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20
Q

hypercoagulable states can be acquired or genetic. what are the high risk acquired states?

A 
Myocardial infarction
Immobilisation
Tissue damage 
Cancer
Prosthetic heart valves
DIC
Heparin induced thrombocytopenia
Antiphospholipid syndrome
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21
Q

what is disseminated Intravascular coagulation (DIC) ?

A

is a serious disorder in which the proteins that control blood clotting become over active. Causes.

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22
Q

what is Heparin-induced thrombocytopenia (HIT) ?

A

development of thrombocytopenia (a low platelet count), due to the administration of heparin.

HIT is caused by the formation of abnormal antibodies that activate platelets.

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23
Q

hypercoagulable states can be acquired or genetic. what are the lower risk acquired states?

A 
Atrial fibrillation
Cardiomyopathy
Nephrotic syndrome
Hyperoestrogenic states
Oral contraceptive use
Late pregnancy
Sickle cell anaemia
Smoking
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24
Q

hypercoagulable states can be acquired or genetic. What are the genetic states?

A
  • Factor V mutations (2-15% of Caucasians)
  • Defects in anticoagulant pathways – antithrombin III deficiency, protein C or S deficiency
  • Defects in fibrinolysis
  • prothrombin 20210 mutation and others
    there is a synergy in these
25
Q

where are the common site of arterial thrombus?

A

coronary, cerebral and femoral

26
Q

what are arterial thrombi associated with?

A

atheroma

27
Q

Arterial thrombi

  • they often ____ the lumen
  • they show ____ attachment to the wall
  • They also show lines of_____
A
  • they often occlude the lumen
  • they show firm attachment to the wall
  • They also show lines of Zahn
28
Q

what are the main causes of mural thrombi in the ventricles?

A

MI, arrhythmias

29
Q

what are the main causes of mural thrombi in the aorta?

A

atheroma

30
Q

what causes mural thrombi to show lines of zahn?

A

Laminated due to alternating pale (platelet & fibrin) and dark (RBC/WBC) bands

31
Q

what component of virchow’s triad is most often implicated in venous thrombosis?

A
  • venous stasis
32
Q

what does venous thrombi often evoke?

A

inflammation - phlebothrombitis

33
Q

where are the common places for venous thrombi?

A

popliteal, femoral, iliac, pelvic

34
Q

what are Large vessel thrombi prone to do?

A

embolise

35
Q

what colour are venous thrombi?

A

reddish blue and are adherent to the wall

36
Q

what are the fates of thrombi? name 4

A

Propagation proximally (small to large vessel)

Embolisation

Resolution (fibrinolysis)

Organisation (granulation tissue, recanalisation)
[DIC]

37
Q

what are the types of embolism/

A 
Thromboembolism
Fat embolism
Marrow embolism
Air embolism
Septic embolism
Amniotic fluid embolism
Tumour embolism
38
Q

where do most PEs arise from?

A

large leg veins (popliteal, femoral, iliac)

39
Q

what shape of infarction do PE normaly cause?

A

wedge shape

40
Q

what colour are PE infarctions and why?

A

haemorrhagic so they are red - this is because lung has two circulations - pulmonary and also oxygenated circulation from bronchial arteries

41
Q

do venous emboli cause infarcts in peripheral arterial circulation?

A

no unless you have a Atrial/Ventricular Septal Defect

42
Q

why would someone get a fat embolism ?

A

over time long bones become more fatty and if the bones have been fractured e.g. during major soft tissue trauma, then the fat can embolise

43
Q

where do most fatty marrow emboli go?

A

to the lungs but some reach the peripheral circulation leading to skin rashes and CNS confusion

44
Q

what may cause gas/air embolism?

A
  • barotrauma
  • Occurs during delivery or abortion
  • Iatrogenic
  • Many anecdotal cases
45
Q

how much gas is required to enter venous circulation?

A

100ml

46
Q

where do the air bubbles occlude?

A

the major vessels

47
Q

what causes amniotic fluid embolism . It is rare

A

Amniotic fluid and debris enters torn veins and embolises to lungs.

48
Q

what does an amniotic embolism cause?

A

marked oedema, often DIC (leading to haemorrhage)

49
Q

where do most systemic emboli come from?

A

heart chambers or on valves

50
Q

give examples of causes of systemic emboli?

A

Arrhythmias - AF
Mural thrombus post MI
Aneurysm

51
Q

what do systemic emboli cause?

A

gangrene, CVA, visceral - very painful

52
Q

what is Monckeberg Medial Calcific Sclerosis

A

Calcification of medium sized arteries in those >50yrs.

53
Q

what is arteriolosclerosis?

A

Small arteries and arterioles
Hyaline and hyperplastic types
Associated with diabetes mellitus and hypertension

54
Q

what are some outcomes of atherosclerosis?

A 
MI 
PVD - gangrene
Mesenteric artery occlusion
Ischaemic encephalopathy (dementia) 
Aortic aneurysm
55
Q

what are the risk factors for atherosclerosis

A 
Age
Sex
“Genetics”
Hypertension
BP 160/95 → 5 x increased risk of IHD
Smoking 
Increases IHD by 70-200%
Diabetes
Increases risk of MI by 2x
Increases risk of gangrene by 8x – 150x
Hyperlipidaemia
Positive association with LDL
Negative association with HDL
56
Q

other risk factors for atherosclerosis?

A 
Lack of Exercise
Obesity
Induces H-T, DM, hypertriglyceridaemia, reduced HDL
High Carbohydrate Diet
Saturated Fats/Trans(unsaturated)Fats
Oestrogenic status
Post-menopausal
Oral Contraceptive Pill
Stress
[Protective role of Alcohol]
57
Q

where is atherosclerosis distributed commonly?

A 
Thoracic aorta
Mainly arch branch points
Carotid artery bifurcations
Especially internal carotid
Circle of Willis 
Coronary arteries
Particularly ostia
Left anterior descending
Arms and associated vessels normally clear
58
Q

what happens next in atherosclerosis?

A

can get resolution, repair (stabalisation by fibrosis and eventually calcification) or complication

59
Q

what complications can you get?

A

1.Ulceration of atheromatous plaque and thrombosis
2- also can get Haemorrhage into plaque with plaque rupture and embolism of plaque contents
Ongoing narrowing → critical stenosis
Aneurysm formation

Cardiovascular: pathology (2 decks)

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