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BDS2 BAMS > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

arteriosclerosis

A

process occurs with aging, deposition of amyloid, hyperplasia of smooth muscles, effects small BVs more

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2
Q

atherosclerosis

A

Can occur at any age (mainly elderly)

deposition of cholesterol on vessels - mainly larger vessels
- plaque build up

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3
Q

what causes nearly half of all deaths in the Western World?

A

artherosclerosis

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4
Q

which types of factors cause arteriosclerosis?

A

its is multifactorial so both modifiable (lifestyle) and non-modifiable factors can cause atherosclerosis

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5
Q

modifiable factors

A

lifestyle (smoking, diet, obesity etc)

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6
Q

non-modifiable factors

A

genes (DNA), age, gender

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7
Q

what is the most important risk factor in atherosclerosis?

A

Hyperlipidaemia

High cholesterol

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8
Q

what are the 2 processes in atherosclerosis?

A

Achronic inflammatory process followed by healing response

Chronic inflammatory process
- Initiates an inflammatory reaction as cholesterol deposited in not correct place

Followed by healing process - but doesn’t heal

Formation of an atheroma

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9
Q

what is an atheroma?

A

a.k.a. a plaque
forms as a result of the artherosclerosis process

  • Has a gruel like texture
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10
Q

define vascular pathology

A

either stenosis/obstruction or to weakening of the walls leading to dilatation/rupture

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11
Q

define stenosis

A

narrowing of blood vessel

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12
Q

define aneurism

A

weakening of vessel wall leading to rupture

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13
Q

non-modifiable factors of atherosclerosis

A
  • age
  • gender
  • genes
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14
Q

age impact on athersclerosis

A

older are more likely to get

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15
Q

gender impact on athersclerosis

A

Males higher than females (before menopause low risk of many cardiovascular disease as oestrogen binds to BV keeping them open) age determines risk factor

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16
Q

genes impact on atherosclerosis

A

Familial hypercholesterolaemia. (Mutation of LDL receptor gene.)
- LDL receptor gene is an Autosomal dominant condition

Liver cells take up circulating LDL of bad cholesterol

Heterozygote - one mutant and one normal gene (50% increase in level of circulating LDL)
- Higher risk of cardiovascular disease

Very high cholesterol level if both mutated - need statins from early age
- Some families have this trait - more risk

LDL receptors present in many cell types including smooth muscle cells, fibroblasts and adrenocortical cells.

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17
Q

2 endothelial cell states

A
  • basal state (normal)

- activated state (pathology)

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18
Q

features of basal (normal) endothelial cell

A
  • Smooth

- non-adhesive and non-thrombogenic surface

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19
Q

features of activated (pathology) endothelial cell

A
  • Initiates lots of different changes cause of change in BV walls
  • increased expression of procoagulants, adhesion molecules and proinflammatory factors
  • altered expression of chemokines, cytokines and growth factors
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20
Q

when will we have basal (normal) endothelial cells?

A
  • Lines our blood vessels
  • when Normal BP in normal range - normal state (no trauma or insult)
  • laminar flow
  • growth factors (e.g. VEGF)
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21
Q

when will we have activated (pathology) endothelial cells?

A
  • turbulent flow
  • hypertension
  • cytokines
  • complement
  • bacterial products
  • lipid products
  • advanced glycation end-products
  • hypoxia, acidosis
  • viruses
  • cigarette smoke
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22
Q

2 basic stages of atheroma formation

A
  • chronic inflammation stage

- healing response phase

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23
Q

chronic inflammation stage of atheroma formation

A

Chronic inflammatory response to lipoproteins

  • Something causing damage to endothelial cells - changing receptors - changing permeability
  • High levels of cholesterol

Endothelial cells change surface cell receptors and become more permeable to lipids.
- Lipids move into tunica intima (first BV layer)

Change cell adhesion molecules for monocytes so attach
to endothelium and move into blood vessel walls.
- Macrophages are the first cell there
- Easier for inflammatory cells to move from blood to vessel walls

Monocytes include macrophages and T-cells.

Foam cells, lipid deposits from dead cells.

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24
Q

healing response phase of atheroma formation

A

Proliferation of smooth muscle cells

Fibrous tissue formation
- More division of fibroblasts and inflammatory cells - viscous cycle (brought in by macrophage and fibroblasts

Growth factors such as PDGF, FGF, TGF-α, are produced.

A fibro fatty plaque is formed with a central mass of lipid and necrotic tissue.

Neovascularization may be seen at the periphery of the plaque.

Haemorrhage can occur into the plaque.

Calcification of the lipid and necrotic tissue may sometimes occur
- Increase in size of atheroma – fatal consequence

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25
Q

5 steps of the atheroma formation process

A
  1. Chronic endothelial cell injury may be genetic mutation, inherited, hypertension etc.
  2. Permeability increases. lipid is deposited in the intimal layers.
  3. Macrophages move in.
    - Foam cells
    - Fatty streaks
    - May regress
  4. Smooth muscle proliferation
    - Macrophages produce IL-1 which activates T-cells.
    - More cytokines, chemokines, ROS activate more inflammatory cells
    - PLGF, FGF, TGF-α,
  5. Fibrous tissue formation, over the lipid and a fibro fatty atheroma is formed (plaque)
    - Dystrophic calcification may occur at late stages
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26
Q

what happens to the lumen of the blood vessel as a consequence of atheroma formation/

A

shrinks (as increased tunica media)

so not enough room for blood transportation

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27
Q

what is the effect of atherosclerosis?

A

decreased blood supply to tissue/organ (ischemia)

thrombosis on top of atheroma and embolisms break off

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28
Q

the effect of atherosclerosis depends on what?

A
  • size of BV
  • extent of obstruction
  • organ effected
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29
Q

what does complete occlusion of the blood vessel lead to?

A

infarction (cell death)

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30
Q

what does partial occlusion of the blood vessel lead to?

A

Less O2, nutrient to cell – ischemia

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31
Q

what is a dental condition that could be caused as a result of atherosclerosis?

A

death of the pulp is blockage of vessel supplying the pulp
(external carotid –> maxillary –> anterior superior alveolar artery, the middle superior alveolar artery and the posterior superior alveolar artery.)

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32
Q

peripheral vascular disease

A

Effects BV all over body

- In particular legs

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33
Q

effects of peripheral vascular disease

A
  • ischemia
  • claudication
  • gangrene
  • coagulation necrosis and infection
34
Q

claudication

A

pain of cramps released by rest

35
Q

aneurysms

A

abnormal dilation, caused by a localised, abnormal, weak spot on a blood vessel wall

  • Can occur in blood vessel or in the cardiac wall as well as other places in the body.
36
Q

what can cause aneurysms

A

number of factors

  • developmental
  • degenerative
  • traumatic
  • infections
37
Q

what type of aneurysms are the commonest?

A

abdominal aortic aneurysms (AAAs)

38
Q

what can be a consequence of an aneurysm?

A
  • peripheral vascular disease
  • ruptured vessels

Widening of lumen of blood vessel - walls become weak
- Release MMPs
- Dangerous as thinning and weakening of BV can result in rupture
Can develop in cardiac wall

39
Q

angina pectoris

A

medical term for chest pain or discomfort due to coronary heart disease. It occurs when the heart muscle doesn’t get as much blood as it needs

40
Q

process of angina pectoris

A
  • Atherosclerosis in BV (particularly coronary arteries), decrease in O2 and nutrients to myocardial tissue

Inc in metabolic demands of heart (activity, shock, emotions) can cause angina pectoris

41
Q

treatment for angina pectoris

A

Take medication and rest and usually resolved

42
Q

myocardial infarction

A

Complete obstruction to myocardial muscle (necrosis)

- Infarction-loss of blood supply; oxygen; nutrients

43
Q

what occurs to the myocardial muscle as a result of myocardial infarction?

A

coagulation necrosis

  • Outline of cell the same, nuclei’s smaller and breaks up so disappears
  • Only have outline of cell left

and if survive then healing by granulation tissue
- fibrous tissue (different function)

44
Q

why is anaerobic respiration ineffective for myocardial muscle?

A

lasts only a few mins cannot keep up with high metabolic demands of heart

45
Q

what happens to cells in coagulation necrosis

A

Cells retain outline so can be identified
- brighter, muscle striations gone

Cytoplasm becomes darker

Remains of nuclei

Striations lost

Inflammatory cells

  • Beginning of inflammation and tissue
  • Neutrophils the first to arrive
  • Then macrophage later - phagocytosis - take away necrotic tissues
  • No more empty spaces

Granulation tissue

  • macrophages, fibrous tissue replaces muscle fibres (collagen made from fibroblasts) capillaries - blood (rapidly dividing cells)
  • Number of BV decrease as inflammation decreases, less muscle mainly fibrous tissue
46
Q

what are the inflammatory cells which arrive during coagulation necrosis and in which order?

A
  • Neutrophils the first to arrive
  • Then macrophage later - phagocytosis - take away necrotic tissues
    No more empty spaces in tissue
47
Q

2 acute coronary syndromes

A
  • angina pectoris

- myocardial infarction

48
Q

what is a chronic coronary syndrome?

A

congestive heart failure

49
Q

congestive heart failure usually follows on from…

A
  • ischemic heart disease (coronary heart disease)
  • hypertension
  • valvular heart disease
50
Q

what happens in congestive heart failure?

A
  • ventricular hypertrophy
  • oedema (at extremities e.g. ankles)
  • chronic venous congestion (CVC) of lung and liver (depending on side of heart which has the failure)
51
Q

what is chronic venous congestion?

A

increased volume of blood in a particular tissue

- Passive process which is the resulting from impaired outflow from a tissue

52
Q

pathophysiology of congestive heart failure

A

Hypertrophy of myocyte (adaptation)

  • resistance of forward flow of heart into circulation
  • Heart needs to pump stronger with more force
  • Become larger in size (not hyperplasia)
  • 2/3 times thicker of normal thickens of ventricular wall

Capillaries do not increase in number

Heart may reach 2-3 times weight of normal

Increased metabolic demands; ischemia.(as cells larger)

Injury to myocyte as a result of ischemia

Apoptosis, heart failure

53
Q

3 pathologies of blood vessels

A
  • Hamartomas
  • kaposi sarcoma
  • angiosarcoma
54
Q

what are the features of Hamartomas?

A
  • Developmental

- Normal tissue in abnormal site or number

55
Q

where do most haemangiomas occur?

A

60% in head and neck

56
Q

what are haemangiomas?

A

Collection of blood vessels (types of hamartoma)

  • Large red fleshy swelling in head and neck
  • Alarming for parents

rapid growth during the first few weeks of life
usually regress over the first 10 years
- usually begin regress after 6 months

don’t disappear – left with red lump/mark

57
Q

what are the 3 types of vascular malformations?

A
  • capillary (lots of little capillaries)
  • cavernous (larger spaces filled with BVs)
  • Sturge Weber Syndrome
58
Q

valscular malformations

A
  • Common haemangiomas
    dark purple bulges on mucosa
  • Present at birth and persist during life.

May become more noticeable in elderly

  • oral mucosa becomes thinner (atrophy) much more noticeable
  • Trauma can cause them to bleed in size - increase in size

Intraosseous malformations may occur

59
Q

sturge weber syndrome

A
  • Extrinsic haemangioma formations
  • Extend to mid line but don’t cross
  • Distribution follows nerves
    E.g. trigeminal in face
60
Q

why is a haemangioma in the jaw bone bad?

A

extraction with lake of blood under

- need specialised hospital setting

61
Q

aetiology of kaposi sarcoma

A

Herpes virus 8 (HHV-8)

62
Q

what is kaposi sarcoma?

A

Multi-focal low-grade sarcoma of lymphatics and blood vessels
- Almost all oral KS are in HIV-infected patients.

63
Q

what is the treatment like for kaposi sarcoma?

A

treatment 90% of cases are controlled (still present)

Immune deficiency- role in carcinogenesis
- Healthy immune reaction is important for control of many viruses - esp oncogenic viruses
Immune suppression due to organ transplant is a risk

64
Q

what is angiosarcoma?

A

many malignant tumour cells and blood vessels

  • rare
  • aggressive cancer
65
Q

benign cardiac tumours

A

myxoma
lipoma

rare

66
Q

malignant cardiac tumours

A

angiosarcoma

rare

67
Q

a way in which cardiac tumours can arise

A

Local extension of tumours from the thoracic cavity such as bronchogenic carcinoma
- Can be around the heart and spread into the heart itself

68
Q

how can someone get valvular heart disease?

A
  • Congenital or acquired

Acquired may be a result of other cardiac diseases such as ventricular hypertrophy

69
Q

what can valvular heart disease pathology result in?

A

Stenosis (injury to valve)

  • Cannot open properly
  • Forward flow impaired

Insufficiency (many causes)

  • Closing of valve impaired
  • Regurgitation of blood back into the chamber it came from

Vegetations.
- Lumps on cusps of valves

70
Q

what is the commonest of all valvular conditions?

A

calcific aortic stenosis

71
Q

process of calcific aortic stenosis

A

Dystrophic calcium deposits as a result of tissue inflammation, hyperlipidaemia.

  • Tissue damage on valves
  • Calcium deposited here due to inflammation

Narrowing of the valvular orifice
- Valve needs to be thin to function properly – stiff now (difficult to open and close)

72
Q

treatment of calcific aortic stenosis

A

valve replacement

need to be on anticoagulants (can lead to bleeding on treatment)

73
Q

what is calcific aortic stenosis

A

Dystrophic calcium deposits as a result of tissue inflammation, hyperlipidaemia.

74
Q

what is rheumatic heart disease a result of?

A

rheumatic fever

rare in the western world

75
Q

what does rheumatic heart disease mainly effect?

A

valves

cross reaction between immune system and valves of heart

76
Q

what is rheumatic heart disease?

A

cross reaction between immune system and valves of heart
- Host immune reaction against Streptococcus A antigens that cross react with host proteins
(Antigens formed against Strep A)

Damage caused by a combination of type 2 (antigen-antibody) and 4 (cell mediated reactions) reactions

77
Q

results of the cross reaction between immune system and valves of heart in rheumatic heart disease

A
  • Inflammation (macrophages and lymphocytes) of endocardium and valves results in fibrinoid necrosis on the surface
  • Vegetations formed along the lines of closure
  • Thickening and fusion , calcification of valves
  • Aortic dilation; atrial fibrillation, thrombi formed on wall of atrium
  • Susceptible to developing infective endocarditis (likely)
78
Q

what is infective endocarditis?

A

Microbial infection of heart valves

Source can come from oral cavity - poor oral hygiene
- Oral pathogens may be implicated

Streptococcus viridens; Staphylococci aureus

79
Q

what valves are particularly susceptible to infective endocarditis?

A

damaged or prosthetic valves

80
Q

what forms on the cusps of valves in infective endocarditis?

A

vegetations

contain fibrin, inflammatory cells and infective pathogens

  • Soft and friable and can break of and enter circulation to infect other areas of body
  • Can cause infective emboli

BDS2 BAMS (54 decks)

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