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BDS2 - cardiovascular medicine > Pathology of CVS > Flashcards

Pathology of CVS Flashcards

1
Q

what is arteriosclerosis

A

the thickening and hardening of the walls of the arteries, occurring typically in old age

  • not as big a concern
  • mainly affects small blood vessels
  • hyperplasia of smooth muscles
  • inflammation
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2
Q

what is atherosclerosis

A

a disease of the arteries characterised by the deposition of fatty material on their inner walls.

a chronic inflammatory process followed by healing response

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3
Q

what are non-modifiable factors that cause atherosclerosis

A
  • genes
  • gender
  • age
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4
Q

what are lifestyle choices that cause atherosclerosis

A

smoking
diet
obesity

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5
Q

what is hyperlipidaemia

A

an abnormally high concentration of fats or lipids in the blood.

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6
Q

what is the most important risk factor of atherosclerosis

A

hyperlipidaemia

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7
Q

what is formed in atherosclerosis

A

an atheroma

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8
Q

what size of blood vessels does atherosclerosis usually affect

A

larger blood vessels

coronal vessels

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9
Q

what is vascular pathology

A

either stenosis or obstruction or the weakening of the walls leading to dilation or rupture (aneurism)

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10
Q

what does stenosis mean

A

the abnormal narrowing of a passage in the body

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11
Q

how can genes cause atherosclerosis

A

> familial hypercholesterolaemia = mutation of LDL receptor gene
- LDL = low density lipoprotein (bad cholesterol),
found in liver cells
in healthy people the LDL receptor will take up circulating LDL and process it in the liver
in people with a mutation of this gene it doesnt work as well so the individual is at a higher risk of atherosclerosis

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12
Q

how does gender affect your risk of atherosclerosis

A

males are at a higher risk and women who have undergone menopause

before undergoing menopause women have a high level of oestrogen in the blood which keeps the blood vessels open so they are at a lower risk of getting the disease but after menopause women lose this protection

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13
Q

how does age affect the risk of atherosclerosis

A

older people are more likely to develop this disease so they are at a higher risk
can occur in any age though even children

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14
Q

where are LDL receptors present

A

in many cell types including

  • smooth muscle cells
  • fibroblasts
  • adrenocortical cells
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15
Q

what are endothelial cells like in the basal state (normal)

A

[factors affecting endothelial cells]

  • normotension
  • laminar flow
  • growth factors eg VEGF

[what endothelial cells are like as a result]

  • non-adhesive
  • non-thrombogenic surface
  • smooth cells
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16
Q

what are endothelial cells like in an activated state (pathology)

A

[factors affecting endothelial cells]

  • turbulent flow
  • hypertension
  • cytokines
  • complement
  • bacterial products
  • lipid products
  • advanced glycation end products
  • hypoxia
  • acidosis
  • viruses
  • cigarette smoke

[what endothelial cells are like as a result]

  • increased expression of procoagulants, adhesic molecules and pro-inflammatory factor
  • altered expression of chemokines, cytokines and growth factors
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17
Q

what are the 2 stages of atheroma

A
  • chronic inflammation phase

- healing response phase

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18
Q

what happens in the chronic inflammation phase

A
  • chronic inflammatory response to lipoproteins (something damages the endothelial cells)
  • endothelial cells change surface cell receptors and become more permeable to lipids
  • change cell adhesion molecules for monocytes so attach to endothelium and move into blood vessel walls
  • monocytes include macrophages and T cells
  • macrophages become foam cells and release lipid deposits from dead cells
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19
Q

what happens to macrophages do during the formation of an atheroma

A

they undergo phagocytosis and ingest lipids
they are big and pale in colour
a whole group of these together are called soap cells
lipid can’t be digested by the cell so it remains within the cell until the macrophage dies
then the lipid is released into circulation again

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20
Q

what are foam cells

A

Foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance.
These cells secrete various substances involved in plaque growth and their death promotes inflammation, thereby contributing to cardiovascular disease.

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21
Q

what happens in the healing response phase

A
  • proliferation of smooth muscle cells (tunica media thickening and cap formed over the cholesterol)
  • 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
  • neovascularisation may be seen at the periphery of the plaque
  • haemorrhage can occur into the plaque (increase in size = fatal consequences)
  • calcification of the lipid and necrotic tissue can sometiimes occur
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22
Q

what is the 5 stages within the phases of the formation of atheroma

A
  1. chronic endothelial cell injury
  2. permeability increase
  3. macrophages move in
  4. smooth muscle proliferation
  5. healing process
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23
Q

how can chronic endothelial cell injury occur

A
  • genetic mutation
  • inherited
  • hypertension
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24
Q

what does the increase permeability in the formation of atheroma allow for

A

lipid to be deposited in the intimal layers
allows for movement
causing damage to the endothelial cells

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25
Q

what happens in the formation of an atheroma when macrophages move in

A

foam cells are formed
fatty steaks are formed (yellow streaks in wall of blood vessel)
may regress - if patient is aware and takes the steps to change their risk factors it can at least be held in check

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26
Q

what happen during smooth muscle proliferation during the formation of an atheroma

A

macrophages produce IL-1 which activates T cells

more cytokines, chemokines, ROS activate more inflammatory cells PLGF, FGF, TGF-alpha

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27
Q

what happens in the healing process of the formation of an atheroma

A

fibrous tissue is formed over the lipid
a fibro fatty atheroma is formed (plaque)
dystrophic calcification may occur at late stages

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28
Q

what do the effects of atherosclerosis depend on

A

the size of the blood vessel and the extent of the obstruction and what organ is affected

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29
Q

what are the effects of atherosclerosis

A
  • decreased blood supply to tissue/organ (ischaemia)
  • complete occlusion of the blood vessels lead to infarction
  • thrombosis
  • embolism
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30
Q

how does atherosclerosis cause ischaemia

A

narrowing of the blood vessel

lack of oxygen and nutrients going to the tissues

31
Q

how does atherosclerosis cause infarction

A

if no blood can go through the blood vessel then it will lead to cell death

32
Q

how does atherosclerosis cause thrombosis

A

release of thrombogenic factors so the process of coagulation is set up which cuts off the blood supply
blood clots can then break off and lodge in other vessels and cause more problems

33
Q

what is an embolism

A

obstruction of an artery, typically by a clot of blood or an air bubble
/ the lodging of an embolus (a blockage causing piece of material) inside a blood vessel

34
Q

how is chronic periodonitits a risk factor for atherosclerosis

A

the pathogenic biofilm with bacteria can enter the blood stream

35
Q

what is included in peripheral vascular disease

A
  • ischaemia
  • claudication
  • gangrene
  • coagulation necrosis and infarction
36
Q

what is claudication

A

a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.

37
Q

what is gangrene

A

localized death and decomposition of body tissue, resulting from obstructed circulation or bacterial infection.

38
Q

what is an aneurysm

A

An aneurysm refers to a weakening of an artery wall that creates a bulge, or distention, of the artery.
abnormal dilation
can occur in blood vessels or in the cardiac wall as well as other parts of the body
at the most severe stage can rupture and cause life threatening internal bleeding

39
Q

what can cause an aneurysm

A

a number of factors such as developmental, degenerative or traumatic factors (eg infections)

40
Q

what does AAA stand for and what is it

A

abdominal aortic aneurysms
= commonest aneurysms
= results from atherosclerosis

a bulge or swelling in the aorta, the main blood vessel that runs from the heart down through the chest and tummy
It can get bigger over time and could burst (rupture - walls become weak and thin), causing life-threatening bleeding

play a role in peripheral vascular disease

macrophages in the wall of the blood vessels releases MMPs which break down the fibres in the wall of the blood vessel

41
Q

what are acute coronary conditions

A
  • angina pectoris

- myocardial infarction

42
Q

what is angina pectoris

A

chest pain / discomfort due to coronary heart disease
occurs when the heart muscle doesn’t get as much blood as it needs
can be caused by ischaemia
usually taken as a warning sign of being at risk of a stroke or heart attack

43
Q

how can you treat angina pectoris

A

medication and rest

44
Q

what does infarction mean

A

loss / obstruction of the blood supply to an organ or region of tissue

45
Q

what is myocardial infarction

A

coagulation necrosis of myocardial muscle
a condition of cell death that is caused by lack of blood flow which can occur in any cell in the body
anaerobic respiration is ineffective
healing by granulation tissue which affects the heart function

46
Q

why is anaerobic respiration ineffective a cause of myocardial infarction

A

cardiac muscle tries to do this method of respiration to compensate for being unable to carry out aerobic respiration due to the lack of oxygen supply
doesnt last for more than a few minutes as it cannot keep up with the high demands of the cardiac muscle
death of part of myocardial muscle

47
Q

how does the body try to heal a myocardial infarction

A

replacement of the dead muscle with fibrous tissue

fibrous tissue wont have the same function so the heart cannot return to normal

48
Q

what happens histologically in coagulation necrosis

A

cells retain outline so can be identified ie will still be able to tell it is cardiac muscle
cytoplasm becomes darker
remains of nuclei
striations lost
inflammation cells (neutrophils are the first to arrive followed by macrophages = phagocytosis to try and remove necrotic tissue)
granulation tissue components

49
Q

what does the process of healing involve in coagulation necrosis

A 
first tissue formed is granulation tissue
replace muscle fibres
fibrous tissue is formed by fibroblasts
removal of dead tissues
number of blood vessels decreases
inflammation decreases
more collagen fibres 
less fibroblasts
50
Q

what are examples of chronic coronary syndromes

A
  • congestive heart failure (usually follows IHD, hypertension or valvular heart disease)
  • ventricular hypertrophy
  • oedema
  • chronic venous congestion (CVC) of lung and liver
51
Q

what is the pathophysiology of chronic coronary syndromes

A
  • hypertrophy of myocyte (adaptation) so heart needs to pump stronger and more force is needed for the blood to circulate
  • capillaries do not increase in number (cells get bigger but do not increase in number) so there is not an increase in blood flow and the larger myocytes means there is little space left for the blood to be present
  • heart may reach 2-3 times the weight it normally is as the muscle is larger in size and functioning more and needing more energy
  • this increases the metabolic demands and leads to ischaemia
  • injury to the myocyte as a result of ischaemia
  • heart failure because of necrosis of tissue
52
Q

what is apoptosis

A

programmed cell death

53
Q

what are tumours of the blood vessels

A
  • hamartomas
  • kaposi sarcoma
  • angiosarcoma (rare and aggressive)
54
Q

where would you find a textbook haemangioma

A

new born infants
have a large raised fleshy swelling when born
very soft and can bleed quickly

55
Q

what is a haemangioma

A
  • type of hamartoma
  • 60% in head and neck
  • rapid growth during the first few weeks of life
  • usually regress over the first 10 years
  • after 6 months become more fibrous
  • dont disappear altogether, a small red mark remains
56
Q

what are vascular malformations

A
  • common
  • present at birth and persist during life
  • noticeable in elderly (mucosa become thinner [atrophy] when you are older so if a person has one it is easier to see)
  • trauma causes these to bleed / become larger
  • intraosseous malformations may occur
57
Q

what are the types of vascular malformations

A
  • capillary
  • cavernous
  • struge weber syndrome
58
Q

where are cavernous haemangioma common

A

midline of face

follows distribution of nerves

59
Q

what is the struge weber syndrome haemangioma / vascular malformation

A

extesnive haemangioma for most part of the oral cavity
may also be present in the jaw bone
most likely to be treated for invasive dental treatment in a specialised hospital setting

60
Q

what is a kaposi sarcoma

A
  • aetiology = herpe virus 8 (HHV-8)
  • multi-focal low-grade sarcoma of lymphatics and blood vessels
  • almost all oral KS are hiv-infected patients
  • treatment in 90% of cases are controlled (doesnt go away)
  • virus has the ability to produce this malignancy in people who are immune suppressed so it highlights the importance of the immune response
61
Q

what is angiosarcoma

A
  • rare
  • aggressive cancer
  • malignant endothelial cells
62
Q

what are cardiac tumours

A
  • rare
  • benign such as myxoma or lipoma
  • malignant such as angiosarcoma
  • local extension of tumours from the thoracic cavity such as bronchogenic carcinoma (areas surrounding the heart spread into heart)
63
Q

how can valvular heart disease develop

A

can be congenital or acquired

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

64
Q

valvular heart disease pathology of the valves result in

A
  • stenosis
    = injury to valve
    = valve cannot open properly
  • insufficency
    = many causes
    = closing of the valve impaired
    = regurgitation of the blood back into the chamber from which it left
  • vegetations
    = little lumps
65
Q

what is calcific aortic stenosis

A
  • commonest of all valvular conditions
  • dystrophic calcium deposits as a result of tissue inflammation, hyperlipidaemia
  • needs valve replacement
  • can occur inflamed and damaged tissue
  • dystrophic calcifications
    [> formed within valves,
    > valves should be thin,
    > as a result of this they become thick and stiff,
    > difficulty in opening and closing]
66
Q

what results from rheumatic fever

A

rheumatic heart disease

67
Q

what happens in rheumatic heart disease

A
  • mainly affects the valves
  • host immune reaction against streptococcus A antigens that cross react with host proteins
  • damage caused by a combination of type 2 and type 4 reactions (hypersensitivity reactions)
  • inflammation of endocardium and valves results in fibrinoid necrosis
  • vegetations formed along the lines of closure (swelling)
  • thickening and fusion, calcification of valves
  • aortic dilation (atrial fibrillation, thrombi formed on wall of atrium)
  • susceptible to developing infective endocarditis
68
Q

what is infective endocarditis

A

microbial infection of heart valves

69
Q

what are susceptible to infective endocarditis

A

damaged or prosthetic valves

70
Q

what can cause infective endocarditis

A

oral pathogens
> Streptococcus viridens
> staphylococci aureus
Found in mouth due to bad oral hygiene

71
Q

what do vegetations found on the cusps in infective endocarditis contain

A

fibrin
inflammatory cells
infective pathogen

72
Q

what can infective endocarditis cause

A

Can cause infective emboli

problems in other organs in other parts of the body

73
Q

who does leanne kiss on the daily?

A

ben scott, heres his snapchat incase you forgot ;) ben0scott0

BDS2 - cardiovascular medicine (2 decks)

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