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EMS > Lecture 9 - Atheroma, thrombosis and embolism > Flashcards

Lecture 9 - Atheroma, thrombosis and embolism Flashcards

1
Q

What do Atheroma, thrombosis and embolisms cause?

A

Major cause of morbidity and mortality
Myocardial infarction
Cerebral infarction
Pulmonary embolism

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2
Q

what is an atheroma?

A

Intimal lesion that protrudes into a vessel wall. It consists of a raised lesion with a soft core of lipid (mainly cholesterol and cholesterol esters) and is covered by a fibrous cap.

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3
Q

What is found in the fibrous cp?

A

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin

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4
Q

what is found in the necrotic centre?

A

Cell debris, cholesterol crystals, foam cells, calcium
(Can become calcified)

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5
Q

what are foam cells?

A

Macrophages that engulf the lipids

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6
Q

What do you get excess lipid in atheroma development?

A

Macrophages absorb lipids and turn into foam cells however they are good at absorbing it so there is left over lipids.

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7
Q

What are some commonly affected vessels of atheroma?

A

Bifurcations (sites of turbulent flow)
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid vessels
Circle of Willis

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8
Q

What are some non- modifiable risk factors?

A

Increasing age
Male gender
Family history
Genetic abnormalities

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9
Q

What are some modifiable risk factors?

A

Hyperlipidemia (LDL: HDL)
Hypertension
Cigarette smoking
Diabetes
C-reactive proteins

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10
Q

What does atherosclerosis start with?

A

Atherosclerosis starts with damage or injury to the inner layer of an artery.

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11
Q

What can damage to the inner layer of an artery be caused by?

A

High blood pressure
High cholesterol
An irritant, such as nicotine
Certain diseases, such as diabetes

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12
Q

How does atherosclerosis develop in response to endothelial injury?

A

Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury.

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13
Q

How does lesion progression occur?

A

Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall.

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14
Q

How is the contemporary view of atherosclerosis expressed?

A

response-to-injury hypothesis

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15
Q

What are the steps after the response to injury in atherosclerosis?

A
  1. Endothelial dysfunction (Increased permeability, leukocyte adhesion, monocyte adhesion and emigration)
  2. Smooth muscle emigration from media to intima. Macrophage activation.
  3. Macrophages and smooth muscle cell engulf lipid
  4. Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
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16
Q

What is the fatty streak?

A

The earliest lesion in atherosclerosis
Composed of lipid filled foamy macrophages
Begins as multiple minute flat yellow spots that eventually coalesce into streaks >= 1cm
These lesions are not significantly raised and do not cause flow disturbance

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17
Q

Do all fatty streaks form a plaque?

A

Not all fatty streak are destined to progress to atheromatous plaque

Nevertheless coronary fatty streaks begin to form in adolescence at the same anatomical sites that later tend to develop plaques

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18
Q

Atherosclerotic plaque characteristics?

A

Consists of intimal thickening and lipid accumulation
Appears white yellow and superimposed thrombus on the plaque appears red
Plaque impinges on the vessel lumen

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19
Q

Sequelae of atherosclerosis:

A

Rupture, ulceration or erosion of the intimal surface exposes the blood to highly thrombogenic substances and induces thrombosis… Lumen occlusion…ischemia
Haemorrhage into plaque
Atheroembolism
Aneurysm formation

20
Q

what is a thrombus?

A

A solid mass of blood constituents formed within the vascular system in vivo

21
Q

What is the most common cause of arterial thrombosis?

A

Arterial thrombosis most commonly superimposed on atheroma

22
Q

What is the most common cause of venous thrombosis?

A

Venous thrombosis is most commonly due to stasis

23
Q

What are the three factors of Virchow’s triad?

A
  1. endothelial injury
  2. Abnormal Blood flow
  3. Hypercoaguliability
24
Q

Mechanism of Arterial thrombosis?

A

Typically from rupture of atheromatous plaque

25
Q

Mechanism of Venous thrombosis?

A

Typically from combination of factors from Virchow triad

26
Q

Location of arterial thrombosis?

A

Left heart chambers, arteries

27
Q

Location of venous thrombosis?

A

Venous sinusoids of muscle and valves of veins

28
Q

Diseases of arterial thrombosis?

A

Acute coronary syndrome
Ischaemic stroke
claudication

29
Q

Diseases of Venous thrombosis?

A

Deep vein thrombosis (DVT)

Pulmonary embolism

30
Q

Composition of Arterial thrombosis?

A

Mainly platelets

31
Q

Composition of Venous thrombosis?

A

Mainly fibrin

32
Q

Treatment of arterial thrombosis?

A

Anti-platelet agents (clopidogrel)

33
Q

Treatment of Venous thrombosis?

A

Anticoagulants (heparin, warfarin)

34
Q

What are the different categories of Hypercoagulability?

A
  1. Hereditary
  2. Acquired
35
Q

Examples of hereditary hypercoagulability factors:

A

Factor V Leiden
Prothrombin G20210A
Protein C and S deficiency

36
Q

Examples of Acquired hypercoagulability factors:

A

Cancer
Chemotherapy
OCR/HRT
Pregnancy
Obesity
HIT

37
Q

Differences between Clots and Thrombus?

A

Clots - platelets not involved whereas in thrombus they are.
Clots occur inside or outside of the vessel where in thrombus it occurs only outside the vessel
Clots are red whereas arterial thrombus are pale.
Clots are Gelatinous whereas thrombus are firm
Clots are not attached to the vessel wall whereas thrombus’ are.

38
Q

Sequence of thrombosis?

A

Occlusion of vessel
Dissolution
Incorporation into vessel wall
Recanalization
Embolization!!!!!

39
Q

what is an embolus?

A

A mass of material in the vascular system able to become lodged in the vessel and block its lumen

40
Q

Where are most emboli derived from?

A

Thrombi

41
Q

what is the most common form of embolus?

A

Most common – pulmonary
embolus derived from
deep vein thrombosis

42
Q

What are the different types of emboli?

A

Thrombus derived
Atheromatous plaque material
Vegetation on heart valves (infective carditis)
Fragments of tumour (causing metastasis)
Amniotic fluid
Gas
Fat

43
Q

What does the severity of an pulmonary embolus depend on?

A

Size of embolus

44
Q

What can a pulmonary embolus cause?

A

Acute respiratory and cardiac problems

Sudden death

45
Q

where does a systemic emboli originate from?

A

Generally originate from the heart or atheromatous plaque

46
Q

What can a systemic emboli cause?

A

CVA, TIA, gangrene, bowel necrosis

Sequelae of myocardial infarction

Atrial fibrillation

Infective endocarditis – heart valve vegetations

EMS (54 decks)

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