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CVS > Atheroma > Flashcards

Atheroma Flashcards

1
Q

What is an atheroma?

A

Formation of focal elevated lesions (plaques) in intima of large and medium-sized arteries

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2
Q

what are the four stages of atheroma?

A

fatty streak
early atheromatous plaque
fully developed atheromatous plaque
complicated atheromatous plaque

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3
Q

fatty streak

  • who’s affected?
  • what is the clinical significance ?
  • what is the appearance ?
  • what causes it?
A

young children are affected
no clinical significance
yellow linear elevation
lipid laden macrophages

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4
Q

what is the definition of a fully developed atheromatous plaque?

A

central lipid core with a fibrous cap, covered by arterial endothelium.

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5
Q

what is the fibrous cap made up of?

A

collagen (made from smooth muscle) and inflammatory cells

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6
Q

what is the central lipid core made up of?

A

cellular lipids and debris derived from macrophages

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7
Q

why are some macrophages “foamy”?

A

due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor

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8
Q

what are three characteristics of late stage development of fully developed atheromatous plaques ?

A

Dystrophic calcification extensive
Confluent
Cover large areas

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9
Q

What three things can make an atheroma complicated?

A
  • Haemorrhage into plaque (calcification)
  • Plaque rupture/fissuring
  • Thrombosis
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10
Q

what is arteriosclerosis ?

A

thickening of the media layer of the blood vessel which can compromise blood flow. (NOT atheromatous)

  • hypertrophy of the smooth muscle
  • duplication of the internal elastic laminae
  • intima fibrosis
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11
Q

what is the biggest risk factor for atheromatous plaques?

A

hypercholestrolaemia

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12
Q

can hyperlipidemia be related to genes?

A

yes

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13
Q

how many caucasians are heterogeneous for the gene mutation when cell membrane receptors for LDLs are absent?

A

1/500

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14
Q

how can chronic hyper cholesterol directly damage endothelium?

A

by increasing the number of reactive oxygen species which creates more foamy macrophages which are toxic to the endothelial cells and release growth factors and cytokines.

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15
Q

state the five main risk factors for hyperlipidemia and other less strong risk factors

A
  • age
  • male
  • smoking
  • hypertension
  • diabetes
  • obesity
  • low birth weight
  • low economic status
  • lack of exercise
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16
Q

what are the three clinical signs of hyperlipidemia ?

A
  • corneal arcus
  • tendon xanthomata
  • xanthelasmata
17
Q

What are the two ways to form an atheroma?

A
  1. injury to endothelial lining of artery

2. chronic inflammatory and healing response of vascular wall to agent causing injury

18
Q

describe the pathophysiology of atheromatous plaques

A
  1. Endothelial injury
  2. Endothelial dysfunction
    - Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
    - High permeability for LDL
    - Increased thrombogenicity
  3. Accumulation of lipoproteins (LDL) in vessel wall
  4. Monocyte adhesion to endothelium → migration into intima and transformation to foamy macrophages (by free radicals)
  5. Platelet adhesion
  6. Factor release from activated platelets, macrophages (tissue factors)→ smooth muscle cell recruitment
  7. Smooth muscle cell proliferation, extracellular matrix production and T-cell recruitment
  8. Lipid accumulation (extracellular and in foamy macrophages)
19
Q

What can occur in a blood vessel when an atheroma ruptures and releases many thrombogenic substances into the blood?

A

the collagen, lipids and debris clot together with platelets and can cause complete occlusion of a vessel which results in reduced blood flow (ischaemia) and may even result in an infarction (necrosis of tissue)

20
Q

give three examples of vessel occlusion consequences

A

MI
stroke
lower limb gangrene

21
Q

what are vulnerable atheromatous plaques?

A

atheromatous plaques the are likely to rupture/ become complicated
thin fibrous cap, large lipid core, prominent inflammation

22
Q

what are the three options for management of atheromatous plaques?

A

prevention

  • smoking cessation
  • control BP
  • weight loss/diet control
  • regular exercise

secondary treatment

  • statins
  • aspirin

surgical options

23
Q

generally what are the common characteristics of highly stenotic atheromatous plaques ?

A

large fibrocalcific component

little inflammation

24
Q

what three substances do plaque inflammatory cells release to increase degradation?

A
  • cytokines
  • proteolytic enzymes
  • reactive oxygen species
25
Q

what three ways are endothelial cells altered when they become injured ?

A

Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL
Increased thrombogenicity

CVS (20 decks)

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