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MoD > L9 - Atheroma, thrombosis and embolism > Flashcards

L9 - Atheroma, thrombosis and embolism Flashcards

1
Q

what is an atheroma?

A

Intimal lesion that protrudes into the vessel wall

  • raised lesion
  • soft core of lipid
  • fibrous cap
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2
Q

what cells would you find in the fibrous cap of an atheroma?

A
  • SMC
  • macrophages
  • foam cells
  • lymphocytes
  • collagen and elastin
  • proteoglycans
  • neovascular
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3
Q

what cells would you find in the necrotic centre of an atheroma?

A
  • cell debris
  • cholesterol crystals
  • foam cells
  • calcium,
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4
Q

which vessels are commonly affected by atheroma?

A

bifications (sites of tubulent flow)

  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • carotid vessels
  • circle of willis
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5
Q

which is the most common site of atheroma?

A

abdominal aorta

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6
Q

what are some non-modifiable risk factors for atheroma?

A
  • increasing age
  • male gender
  • family history
  • genetic abnormalities
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7
Q

are women more or less likely to get atheroma than men?

A

less likely up until menopause

  • then after menopause the risk is equal between men and women
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8
Q

what are some modifiable risk factors for atheroma/atherosclerosis?

A
  • hyperlipidemia
  • hypertension
  • smoking
  • diabetes
  • CRP
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9
Q

why is the CRP protein a risk factor in atherosclerosis?

A
  • usually seen in inflammatory conditions

- can cause damamge to vessel walls = atherogenesis

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10
Q

what is atherogenesis?

A

the formation of fatty deposits in the arteries.

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11
Q

what is atherosclerosis caused by?

A
  • high blood pressure
  • high cholesterol
  • an irritant, such as nicotine (can release free radicals)
  • disease such as diabetes
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12
Q

what is atherosclerosis?

A

Atherosclerosis is a disease in which plaque builds up inside your arteries.

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13
Q

what is atheroma?

A

Intimal lesion that protrudes into the vessel wall

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14
Q

why does atherosclerosis develop?

A

due to chronic inflammatory response of the. arterial wall to endothelial injury

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15
Q

what are the steps of response-to-injury hypothesis?

A
  1. Chronic endothelial injury
  2. Accumulation of lipoproteins
  3. Monocyte adhesion to the endothelium
  4. SMC proliferations and ECM production
  5. factor release
  6. platelet adhesion
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16
Q

in the response-to-injury hypothesis, what occurs due to chronic endothelial injury?

A
  • increased permeability
  • leukocyte adhesion
  • thrombosis
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17
Q

in the response-to-injury hypothesis, what occurs due to the accumulation of lipoproteins?

A

Low-density lipoprotein molecules (LDL) becoming oxidized (LDL-ox) by free
radicals, particularly oxygen free (ROS).

  • When oxidized LDL comes in contact with an artery wall, a series of reactions occur
    to repair the damage to the artery wall caused by oxidized LDL.
  • cholesterol can move in the bloodstream, transported by lipoproteins
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18
Q

in the response-to-injury hypothesis, what occurs due to factor release?

A

Induces SMC recruitment

NB: factors released from activated platelet, macrophages and vascular wall cells

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19
Q

in the response-to-injury hypothesis, what occurs due to SMC proliferations and ECM production?

A
  • artery becomes inflamed
  • cholesterol plaque covers affected area causing:

narrowing of artery

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20
Q

what happens as a result of a narrowed artery?

A

reduced blood flow

increases blood pressure

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21
Q

in the response-to-injury hypothesis, what occurs due to lipid accumulation?

A

gives rise to fatty streaks

evolves into a fibre fatty atheroma

22
Q

what is a a fibrofatty atheroma

A

contains proliferated SMC and has a ECM formed

23
Q

what is a fatty streak?

A

The earliest lesion in atherosclerosis

24
Q

what is a fatty streak composed of?

A

lipid filled foamy macrophages

25
Q

fatty streaks cause flow disturbance, true or false?

A

false

These lesions are not significantly raised and do not cause flow disturbance

26
Q

all fatty streaks progress to atheromatous plaque, true or false

A

false

Not all fatty streak are destined to progress to atheromatous plaque

27
Q

what are the stages of atherosclerosis?

A
  • initial lesion
  • fatty streak
  • intermediate lesion
  • atheroma
  • fibroatheroma
  • complicated lesion
28
Q

describe an initial lesion?

A
  • histologically “normal”
  • macrophage infiltration
  • isolated foam cells
29
Q

describe a fatty streak?

A

mainly intracellular lipid accumulation

30
Q

describe a Intermediate lesion?

A

intracellular lipid accumulation; small extracellular lipid pools

31
Q

what is the Sequelae of atherosclerosis?

A
  1. Rupture, ulceration or erosion of the intimal surface
  2. Haemorrhage into plaque
  3. Atheroembolism
  4. Aneurysm formation
32
Q

what is a Hemostatic plug?

A

a scab formed at the site of vascular injury

33
Q

what is Thrombosis?

A

formation of a blood clot inside a intact blood vessel

34
Q

what is Hemostasis?

A

a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage)

  • maintains blood in fluid state in vessels
  • allows for rapid formation of a homeostatic clot at the site of injury
35
Q

what would inhibit thrombosis?

A

inactivation of Xa and IXa

36
Q

what would promote thrombosis?

A

platelet adhesions

coagulation sequence

37
Q

what is the difference in mechanism behind a arterial thrombosis and a venous thrombosis (VTE)?

A

arterial:
typically from a rupture of a atheromatous plaque

venous:
combination of factors from Virchow triad

38
Q

what is the difference in location between a arterial thrombosis and a venous thrombosis (VTE)?

A

arterial:
left heart chambers, arteries

VTE:
venous sinusoids of muscle and valves of veins

39
Q

what is the different diseases are caused by a arterial thrombosis and a venous thrombosis (VTE)?

A

arterial:

  • acute coronary syndrome
  • ischaemic stroke
  • claudication

VTE:

  • DVT
  • pulmonary embolism
40
Q

what is the difference in composition between a arterial thrombosis and a venous thrombosis (VTE)?

A

arterial:
mainly platelets

VTE:
mainly fibrin

41
Q

what is the difference in treatment between a arterial thrombosis and a venous thrombosis (VTE)?

A

arterial:
anti-platelet agents (clopidogrel)

VTE:
anticoagulants (heparin, warfarin)

42
Q

what type of thrombus would you treat with anticoagulants (heparin, warfarin)?

A

venous thrombosis (VTE)

43
Q

what type of thrombus would you treat with anti-platelet agents (clopidogrel)?

A

arterial thrombosis

44
Q

a thrombosis made up of mainly fibrin would likely be what type of thrombus?

A

venous thrombosis (VTE)

45
Q

a thrombosis made up of mainly platelets would likely be what type of thrombus?

A

arterial thrombosis

46
Q

what are the 3 components of Virchow’s triad?

A

endothelial injury

abnormal blood flow/stasis

hypercoagulability

47
Q

with reference to Virchow’s triad, what factors contribute to abnormal blood flow/stasis?

A

immobility

polycythemia

48
Q

with reference to Virchow’s triad, what factors contribute to hypercoagulability?

A

hereditary:

  • factor V leiden
  • prothrombin G20210A
  • Protein C and S deficiency

Acquired:

  • cancer
  • chemotherapy
  • OCR/HRT
  • pregnancy
  • obesity
  • HIT
49
Q

with reference to Virchow’s triad, what factors contribute to endothelial damage?

A
  • smoking
  • hypertension
  • surgery
  • catheter
  • PICC lines
  • Trauma
50
Q

what is the difference between a clot and a thrombus?

A

clot:

  • platelets not involved
  • occurs outside vessel (hematoma) or inside
  • red
  • gelatinous
  • not attached to a vessel wall

Thrombus:

  • platelets involved
  • only occurs inside a vessel
  • red (venous), pale (arterial)
  • firm
  • attached to vessel wall
51
Q

what is the Sequelae of thrombosis?

A
  • occlusion of vessel
  • dissolution
  • incorporation into vessel wall
  • recanalisation
  • embolism
52
Q

what is an embolus?

A

A mass of material in the vascular system able to lodge in a vessel and block it

NB:

  • May be endo- or exogenous
  • May be solid, liquid or gas

MoD (19 decks)

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