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Medicine 2 - 05 Heart Failure > 6 Vascular Disease: Atheroma and it's complications > Flashcards

6 Vascular Disease: Atheroma and it's complications Flashcards

1
Q

Define arteriosclerosis

A

Thickening and hardening of the wall of an artery

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2
Q

Define Arteriolosclerosis

A

Thickening and hardening of the wall of an arteriole

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3
Q

Define atheroma

A

An important disease with an accumulation of material (fatty) in the wall of large and medium arteries

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4
Q

Define atherosclerosis

A

It is arteriosclerosis due to an atheroma

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5
Q

What is the most common cause of arteriosclerosis in large and medium arteries

A

Atheromas

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6
Q

What is the most common cause of thickening and hardening in the wall of small arteries and arterioles

A

High blood pressure

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7
Q

Describe Hypertensive Atherosclerosis

A

It is the hardening and narrowing of the arteries caused by hypertension

Features:

  • Hypertrophy of tunica media
  • Fibroelastic thickening of tunica intima
  • Elastic lamina is reduplicated

The lumen of the artery is small in size

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8
Q

Describe Hypertensive Arteriosclerosis

A

High blood pressure on arterioles (endothelium, intima, and elastic lamina)
- Replacement of wall structures by amorphous hyaline material

Narrowing + hardening of arterioles, limiting blood flow

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9
Q

List and describe consequences of Hypertensive Vascular Changes

A

Reduction of vessel lumen size
- reduced blood flow
- ischaemia in supplied tissue
- Ischaemia is a lack of blood flow to the supplied tissue/organ - if it reaches a critical level
> can lead to partial/total organ failure (infarction)

Increased rigiity of the vessel wall

  • loss of elasticity
  • unresponsive to normal vessel control agents (e.g. Vasodilators) - over time
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10
Q

Describe Hypertensive Retinopathy as an example of Hypertensive vascular changes

A

Normal retina - clear definition of vessels, macula and optic disc

Abnormal retina - advanced stage Grade 4 Hypertensive Retinopathy

  • Silver wiring of arteries/vessels
  • Where arteries cross veins there is AV nipping
  • Extravasation (blood - flame haemorrhage)
  • Papilloedema - (crisp nature of optic disc is lost)
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11
Q

Describe the effects of atheroma on arteriosclerosis

A

It is the disease of large and medium arteries

  • Only occurs in high-pressure systems e.g. systemic arterial system (not venous system)
  • It is initially a disease of the tunica intima, but later can affect the tunica media

It is ubiquitous, but very mild in young people, worsening with age

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12
Q

Briefly describe the 4 (5) stages of Atheroma formation

A

4 (5) stages:

1 .(technically, initial damage is 1st stage)

  1. Fatty streak (slight discolouration)
  2. Lipid plaque
  3. Fibrolipid plaque
  4. Complicated Atheroma (ulcerated + torn open)
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13
Q

Describe the first stage of Atheroma formation (initial damage)

A

Normal lumen with epithelium

BUT

  • damage can occur
  • leading to high levels of LDL
  • Accumulation of lipids + unhealthy damaged endothelium to enter into the intima
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14
Q

Describe the second stage of Atheroma formation (fatty streak)

A
  • Macrophages come into the area of injury + accumulation of LDL
  • These lipids are phagocytosed by macrophages to make:
    > Raised areas (FATTY STREAK)

This is seen quite commonly in young adults

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15
Q

Describe the third stage of Atheroma formation (lipid plaques)

A

If the fatty streaks continue further

Further injury to endothelium + inflammation (cigarette, tar, stress)

  • There is the continued deposition + accumulation of LDL
  • Some lipid is released by macrophages (too much) - causes LIPID PLAQUE
  • Macrophages secrete cytokines which stimulate myofibroblasts to secrete collagen
  • Collagen deposits in the vessel wall + lumen
  • Leading to early damage to elastic lamina + media
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16
Q

Describe the fourth stage of Atheroma formation (fibrolipid plaque)

A

This collagen and lipid deposition continues
- Now, there is a clear extracellular lipid covering
- Collagen covers plaque surface - FIBROLIPID PLAQUE
- More lipids start to enter
- With a lipid core (may calcify)
(macrophages start to apoptosis)
- Tunica media thins, with replacement of muscle fibres by collagen
- Losing physiological ability of blood vessel (pulsating of blood flow)

There is further encroachment into lumen + vessel

17
Q

Describe the fifth stage of Atheroma formation (complicated atheroma)

A
  • Lipids oxidise + become highly oxidised LDL
    (pro-inflammatory - Calcified and hard)

(the surface - collagenous cap thins, as it can not keep everything trapped in any longer, so the endothelium gives way)
- The fibrolipid plaque ulcerates
> exposing the lipid pool of extracellular lipid, that contains tissue factor (this is the stimulating factor for coagulation)

Ulceration of the endothelium exposes collagen (which contains these tissue factors), where a fibrin-platelet thrombus forms
- Thinning of media leads to weakness and inelasticity ‘COMPLICATED ATHEROMA’

18
Q

List some risk factors that can promote atherosclerosis

A

Smoking
- tar + nicotine content of smoke - promotes atherogenesis
> It can rapidly super oxidise LDL (potent contributor to atherosclerosis)

Diet of saturated fat
Overweight/obesity
Sedentary lifestyle
Lack of exercise (with sedentary lifestyle leads to significant risk factor)

Most of these can be prevented/reduced

Other risk factors:

  • Hypertension
  • Diabetes
  • Hypercholesterolemia (can include those from the above list or even genetics)
19
Q

Describe some complications of atheroma

A
  • Expansion of intima - reduction of the size of the lumen - reduced blood flow + oxygenation of tissue
  • Ulceration of atheromatous intima - predisposition to thrombus formation - vessel occlusion (thromboembolism)
  • Plaque fissure formation + haemorrhage
  • Replacement of muscle + elastic fibres in the media - loss of elasticity - thinning and stretching (aneurysm)
20
Q

What are the consequences of the reduction of the size of the lumen, from atheroma formation?

A

Leads to:

  • Reduced blood flow
  • So reduced oxygenation of tissue, this
  • Ischaemic damage to tissues
21
Q

Describe the different effects of lumen size reduction, based on where the atheroma builds up

A

Coronary arteries
- symptoms of Angina (not permanent damage yet - [MI]

Leg Arteries
- intermittent claudication (pains when walking) -
[LIMB LOSS}

Mesenteric Arteries
- ischaemic colitis (pain in the abdomen)
[INFARCTION]

Cerebral and vertebral arteries
- cerebral ischaemic events (TIA’s - can lead to tissue hypoxia and death)
[STROKE]

SO, if the reduction in the flow of blood is severe enough, tissue may die because of hypoxia [INFARCTION]

22
Q

Describe how an atheroma can be a predisposition to thrombosis

A

Damaged and ulcerated endothelium may lead to the formation of thrombus
- Thrombus may completely occlude the vessel lumen

23
Q

Describe how a plaque fissure can form

A

Blood seeps into atheromatous plaque and expands it
- OR blood seeps into the plaque and undergoes Thrombosis

BOTH can actually occlude the vessel lumen (thrombosis + healing cycle - large rapid growth

24
Q

Give the treatment for atheromatous complications (or formation of atheroma)

A

IN THE PAST
- clot busters like streptokinase were used
BUT there is a downside
- as we are stopping clots from forming, bleeding was occurring in other places like the brain (and px died)

TREATMENT NOW
- Percutaneous Coronary Intervention (PCI)
- Open up the blocked arteries
- Angioplasty and stenting
> Wire in the catheter is passed through vessels to blocked coronary artery
> Balloons used to expand, and stent keeps vessel open
> + whilst restabilising blood flow in coronary arteries

25
Q

Describe the damage to the tunica media as a complication of atheroma

(aneurysm)

A

Enlarging intimal atheroma plaque leads to atrophy of media

  • Muscle and elastic fibres in media is replaced by collagen
  • Collagen is strong but neither contractile nor capable of elastic recoil
  • With each systolic pulse, the wall of the artery stretches and thins, particularly when blood pressure is elevated (this accelerates this whole process)

This leads to the formation of an aneurysm
(most common in the abdominal aorta)

26
Q

Define and describe an Aneurysm

A

An aneurysm is an abnormal permanent focal dilation of an artery
- The most common type of aneurysm (in the abdominal aorta - due to underlying atherosclerosis, which is accelerated by high BP) is secondary to atherosclerosis

Other types occur:

  • Developmental (berry) in cerebral vessels
  • Once aneurysms tear - ‘dissecting aneurysms of the thoracic aorta (very life-threatening)
  • Mycotic aneurysms related to infection (underlying infection is the cause of aneurysm - e.g. infective endocarditis)
  • Syphilitic (not acute infection of syphilis - but chronic later stages of syphilis - aortitis - occlusive inflammation affects vasa vasorum - necrotic death of smooth muscle cells supporting large aorta - loss of integrity, dilation - aneurysmal formation)
27
Q

Describe the 3 different types of aneurysms

A
  • Saccular (growth on one sidewall of the vessel)
  • Fusiform - no one single growth on one side - but generalised dilation on whole blood vessel
  • Dissecting - inner layers of the blood vessel have lost their competency, rapid dilation on the outer layer in media + tearing up of intima and media (very symptomatic + lots of pain)
    > Trying to find ‘true’ and ‘false’ lumen is very hard
28
Q

Describe an abdominal aortic aneurysm

A

Most commonly found the aneurysmal formation

Comprise of organs depends on the location of the aneurysm

  • If it picks of renal artery (compromisation) of kidney blood supply (1 or both)
  • If it picks off too many vertebral arteries - complications of paraplegia
  • Mesenteric or liver infarction
29
Q

Describe syphilitic aneurysm

A

Very rare - with the prolific use of antibiotics (amoxicillin)
- Late complication of syphilitic aortitis
(syphilitic aneurysm)

30
Q

Describe mycotic aneurysms

A

Uncommon

  • mostly caused by endocarditis (infection of the heart valve)
  • Bacterial septicaemia (penetrated into the bloodstream)
  • Infection of arterial wall - in heart valves too

Further weakening and dilation of wall = aneurysm
(risk of bleed)

Medicine 2 - 05 Heart Failure (8 decks)

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