Pathology of cvd Flashcards

1
Q

What is arteriosclerosis?

A
  • A thickening and hardening of the walls of the arteries, occurring typically in old age
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2
Q

What is atherosclerosis?

A

A disease of the arteries characterised by the deposition of fatty materials (cholesterol) on the inner walls

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3
Q

What are 3 examples of ‘non-modifiable factors’?

A
  • Genes
  • Gender
  • Age
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4
Q

The development of atherosclerosis in people is multifactorial. What does it consist of?

A
  • Non-modifiable factors and lifestyle choices (modifiable factors)
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5
Q

What is the most important risk factor of atherosclerosis?

A

Hyperlipidaemia (elevated levels of lipids in the blood plasma)

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6
Q

What is the process of atherosclerosis?

A
  • A chronic inflammatory process followed by the healing response
  • Inflammatory process as cholesterol is deposited in the BV walls (inflammatory reaction of the chronic type)
  • Then healing process - but does not actually heal (you get the response but you don’t get the healting)
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7
Q

What does atherosclerosis cause the formation of?

A
  • An atheroma
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8
Q

What is an atheroma?

A
  • A fatty, fibrous thickening of an artery
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9
Q

What 2 things can a vascular pathology be?

A

Either a stenosis/obstruction or the weakening of the walls leading to dilation/rupture

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10
Q

What is a stenosis?

A
  • An abnormal narrowing of blood vessels
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11
Q

When are females at a higher risk of developing atherosclerosis?

A
  • After menopause - before the onset of menopause women have a lower risk due to BV having a higher level of oestrogen that ensures the BV stays open, however after menopause oestrogen levels decline
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12
Q

What is familial hypercholesterolaemia?

A
  • Autosomal dominant condition
  • Mutation of the LDL receptor gene (low density lipoprotein receptor gene, many cells in the liver have this receptor in the membrane)
  • Cells take up cholesterol from the blood and process it in the liver, if they have one normal gene and one non-functioning gene then they have 50% increase in bad blood cholesterol
  • If they have complete wrong protein have to go on statins as early as possible as at high risk
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13
Q

Where are LDL receptors found?

A
  • Present in many cell types including smooth muscle cells, fibroblasts and adrenocortical cells
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14
Q

What is the chronic inflammation stage of atheroma’s? (5 points)

A
  • Chronic inflammatory response to lipoproteins
  • Endothelial cells change surface cell receptors and become more permeable to lipids
  • Change cells adhesion molecules for monocytes so attach to endothelium and move into blood vessel walls
  • Monocytes include macrophages and T-cells
  • Foam cells, lipid deposits from dead cells
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15
Q

What is a foam cell?

A
  • A foam cell is a specialised type of cell created by white blood cells. Initially a waste removal cell type called a macrophage, the foam cell specifically targets cholesterol and fat build up in the blood cells. Once it has ingested these substances, it assumes a foam like texture and appearance, thereby crating its name
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16
Q

What is the healing response phase of atheroma formation? (7 points)

A
  • Proliferation of smooth muscle cells
  • Fibrous tissue formation
  • Growth factors such as PDGF, FGF, TGF-alpha, 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
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17
Q

What is neovascularisation?

A
  • New blood vessel formation in abnormal tissue or in abnormal positions
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18
Q

What is the overall process of atheroma formation? (5 main points)

A
  1. Chronic endothelial cell injury - may be genet ic mutation, inherited, hypertension etc
  2. PErmeability increases. Lipid is deposited in the intimal layers
  3. Macrophages move in - foam cells, fatty streaks - these may regress if you reduce the risk factors
  4. Smooth muscles proliferation. MAcrophages produce IL-1 which activates T-cells. More cytokines, chemokines, ROS activate more inflammatory cells PLGF, FGF, TGF-alpha
  5. Healing phase - fibrous tissue formation, over the lipid and a fibro fatty atheroma if formed (plaque)
    - Dystrophic calcification may occur at late stages
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19
Q

What are fatty streaks?

A
  • Early evidence of atherosclerosis, macrophages and smooth muscle cells accumulate in the intima of arteries?
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20
Q

What are 4 examples of effects atherosclerosis can have?

A
  • Decreased blood supply to tissue/organ (ischaemia)
  • Complete occlusion of the blood vessel leading to infarction
  • Thrombosis
  • Embolism
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21
Q

What is infarction?

A
  • Obstruction of the blood supply of an organ or region of tissue, causing local death of the tissue
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22
Q

What is thrombosis?

A

When a blood clot forms within a blood vessel and prevents the proper flow of blood around the circulatory system

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23
Q

What is an embolism?

A
  • An obstruction in a blood vessel due to a blood clot or other foreign matter that gets stuck while travelling through the bloodstream
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24
Q

Is chronic periodontitis related to atherosclerosis and CVD

A
  • There is a theory that chronic periodontitis can cause atherosclerosis
  • When a person has CP they have chronic inflammation and lots of factors that are released as a result of this - they are released into the circulation where they travel to the liver and cause an acute phase response which can cause atherosclerosis
  • Still don’t know if this is absolutely true
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25
Q

What 4 things can peripheral vascular disease cause?

A
  • Ischaemia
  • Claudication
  • Gangrene
  • Coagulation necrosis +infection
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26
Q

What is claudication?

A
  • A condition in which cramping pain in the leg is induced by exercise, typically caused by an obstruction of the arteries
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27
Q

What is gangrene?

A
  • Death of the body tissues due to ischaemia
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28
Q

Who is predisposed to gangrene?

A
  • Diabetics
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29
Q

What is coagulation necrosis?

A
  • A condition of cell death that is caused by a lack of blood flow
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30
Q

What is an aneurism?

A
  • An abnormal dilation in the wall of an artery supplying blood to a specific area
  • Can occur in blood vessels or in the cardiac wall as well as other places in the body
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31
Q

What are 3 examples of factors that can cause an aneurism?

A
  • Developmental
  • Degenerative
  • Traumatic
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32
Q

What is the most common type of aneurism and what does this result from?

A
  • AAA’s (abnormal aortic aneurisms)

- Results from atherosclerosis

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33
Q

What do aneurisms play a role in?

A
  • Peripheral vascular disease
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34
Q

Can aneurisms rupture?

A
  • Yes
35
Q

What are 2 examples of acute coronary conditions?

A
  • Angina pectoris

- Myocardial infarction

36
Q

What type of necrosis occurs in myocardial tissue during MI?

A
  • Coagulation necrosis

- The outline of the cell remains the same but the nucleus of the cell will break up and disappear

37
Q

Why does healing of myocardial infarction by granulation tissue affect heart function?

A
  • It is replaced by fibrous tissue which will not have the same function as myocardial tissue
38
Q

What happens to a cell during coagulation necrosis? (6 points)

A
  • Calls retain outline so can be identified
  • Cytoplasm becomes darker
  • Remains of nuclei
  • Striations lost
  • Inflammatory cells - neutrophils first to arrive and followed by macrophages
  • Granlation tissue is the first tissue that is formed
39
Q

Why does granulation tissue contain/produce numerous small blood vessels?

A

To provide a supply of oxygen and nutrients to remove waste

40
Q

What does congestive heart failure usually follow on from? (3 points)

A
  • Ischaemic heart disease
  • Hypertension
  • Valvular heart disease
41
Q

Ventricular hypertrophy occurs with congestive heart failure. What is ventricular hypertrophy?

A
  • An increase in the colume of the myocardium of a ventricle produced entirely by the enlargement of existing cells
  • This is due to chronic pressure overload
42
Q

Oedema occurs with congestive heart failure. What is oedema and where can it be found in this case?

A
  • Oedema = a swelling caused sue to excess fluid accumulation in the body tissues
  • When the heart weakens and pumps blood less effectively, fluid can slowly build up, creating leg oedema. If fluid builds up quickly, you can get fluid in the lungs. IF your heart failure is on the right side of your heart, oedema can develop in the abdomen
43
Q

Chronic venous congestion (CVC) of the lungs and liver occurs with congestive heart failure. What is this?

A
  • Increased volume of blood in a particular tissue is known as congestion. It is a passive process, resulting from impaired outflow from a tissue. It may occur due to generalized cause i.e. in cardiac failure
  • Results due to stagnation of blood because of venous obstruction
44
Q

What is pathophysiology?

A
  • The disordered physiological processes associated with disease or injury
45
Q

What is the pathophysiology of congestive heart failure? (6 points)

A
  • Hypertrophy of monocyte (adaption)
  • Capillaries do not increase in number
  • Heart may reach 2-3 times the weight of normal
  • Increased metabolic demands, ischaemia
  • Injury to monocyte as a result of ischaemia
  • Apoptosis, heart failure
46
Q

What are 3 examples of blood vessel tumours?

A
  • Harmatomas
  • Kaposi sarcoma
  • Angiosarcoma: rare/aggressive
47
Q

What is a hamartoma?

A
  • A noncancerous tumour made of an abnormal mixture of normal tissues and cells from the area in which it grows
48
Q

What is a Kaposi Sarcoma?

A
  • A cancer that develops from the cells that line the blood vessels and the lymphatic system. Kaposi sarcoma usually appears as tumours on the skin or mucosal surfaces such as the inside of the mouth, but these tumours can also develop in other parts of the body such as the lymph nodes or lungs
49
Q

What Is an angiosarcoma?

A
  • A cancer of the inner lining of blood vessels, and it can occur in any area of the body
50
Q

What is a haematoma?

A
  • A hamartoma

- It is a non-cancerous (benign tumour) growth of blood vessels

51
Q

What percentage of haemangiomas are found in the head and neck?

A
  • 60%
52
Q

At what stage of life is there rapid growth of a haemangioma?

A
  • The first few weeks of life
53
Q

At what age/stage of life do haemangiomas usually regress?

A
  • Over the first 10 years
54
Q

What is a vascular malformation?

A
  • A broad term used to refer to abnormalities that affect the vascular system including lymph vessels, arteries and veins
55
Q

Are vascular malformations common?

A
  • Yes
56
Q

Are vascular malformations present at birth?

A
  • Yes, the are congenital so it begins at the time the child is born. However, it doesn’t normally manifest prominently until the baby has entered childhood
  • It develops as a person ages so it pro gresses slowly, though there are times where the growth is quite fast
57
Q

Why may vascular malformations become more noticeable in the elderly?

A
  • There is a change in the mucosa that makes them more noticeable - iral mucosa becomes thinner so they become much more noticeable
58
Q

With vascular malformations, intraosseous malformations may occur, what does this mean?

A
  • Into the bone
59
Q

What are the 3 types of vascular malformations?

A
  • Capillary
  • Cavernous
  • Struge Weber Syndrome
60
Q

What is a cavernous vascular malformation?

A
  • A vascular abnormality characterised by clusters of the blood vessels which are usually enlarged, creating caverns within the cluster through which blood moves very sluggishly
61
Q

What is Struge-Weber Syndrome?

A
  • A vascular malformation
  • Rare condition present at birth that affects the brain, skin and eyes
  • The cause of the syndrome is thought to be an abnormal development of blood vessels in the brain while the baby is in the womb.
  • An additional layer of blood vessels, known as angioma, forms on the outside of the brain, leading to neurological symptoms such as seizures and learning difficulties
  • As development of the brain and skin are closely related, blood vessels in the skin also grow abnormally, causing a birthmark to appear
62
Q

What is the cause (aetiology) of Kaposi Sarcoma’s?

A
  • Herpes virus 8 (HHV-8)
63
Q

What is Kaposi Sarcoma?

A
  • Multi-factorial low grade sarcoma of lymphatics and blood vessels
64
Q

Almost all oral Kaposi Sarcoma’s are found in HIV-infected patients. With treatment, what % of cases are controlled?

A
  • 90%
65
Q

Are cardiac tumours common or rare?

A
  • Rare
66
Q

Give an example of 2 benign cardiac tumours?

A
  • Myxoma

- Lipoma

67
Q

Give an example of a malignant cardiac tumour?

A
  • Angiosarcoma
68
Q

What is a bronchogenic carcinoma?

A
  • Any type or subtype of lung cancer

- Local extension of tumours from the thoracic cavity

69
Q

Valvular heart disease may be congenital or acquired. What may acquired be a result of?

A
  • Result of other cardiac diseases such as ventricular hypertrophy
70
Q

What can valvular heart disease result in? (3 points)

A
  • Stenosis (injury to valve)
  • Insufficiency (many causes) (closing of valve will be impaired)
  • Vegetations - formation of little lumps upon the cusps of the valve
71
Q

What is the most common valvular condition?

A
  • Calcific aortic stenosis
72
Q

What is calcific aortic stenosis?

A
  • Dystrophic calcium deposits as a result of tissue inflammation, hyperlipidaemia
73
Q

What does calcific aortic stenosis cause?

A
  • Narrowing of the valvular orifice
74
Q

With calcific aortic stenosis a valve replacement may be required. What is a concern of this?

A
  • The patient may be on anticoagulants which will result in bleeding from the patients
75
Q

What does rheumatic heart disease result from?

A
  • Rheumatic fever
76
Q

What does rheumatic heart disease mainly affect?

A
  • Valves
77
Q

What is rheumatic heart disease?

A
  • A host immune reaction against Streptococcus A antigens that cross react with host proteins
  • Damage caused by a combination of type 2 and 4 reactions
  • Type 2 - cytotoxic
  • Type 4 - Hypersensitivity
78
Q

How does rheumatic heart disease occur? (5 points)

A
  • Inflammation of endocardium and valves result in fibrinoid necrosis
  • Vegetations formed along the lines of closure
  • Thickening and fusion, calcification of valves
  • Aortic dilation; atrial fibrilation, thrombi formed on wall of atrium
  • Susceptible to developing infective endocarditis
79
Q

What is infective endocarditis?

A
  • Microbial infection of heart valves
80
Q

What type of valves are particularly susceptible to infective endocarditis?

A
  • Damaged or prosthetic valves
81
Q

Oral pathogens may be implicated with infective endocarditis. Give 2 examples of these?

A
  • Streptococcus viridens

- Staphylococci aureus

82
Q

In infective endocarditis, what do the vegetations forms on the cusps pf valves contain? (3 points)

A
  • Fibrin
  • Inflammatory cells
  • Infective pathogens
83
Q

What can infective endocarditis cause what will travel round the body in the blood?

A
  • Infective emboli