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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
what happens in the formation of an atheroma when macrophages move in
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
26
what happen during smooth muscle proliferation during the formation of an atheroma
macrophages produce IL-1 which activates T cells | more cytokines, chemokines, ROS activate more inflammatory cells PLGF, FGF, TGF-alpha
27
what happens in the healing process of the formation of an atheroma
fibrous tissue is formed over the lipid a fibro fatty atheroma is formed (plaque) dystrophic calcification may occur at late stages
28
what do the effects of atherosclerosis depend on
the size of the blood vessel and the extent of the obstruction and what organ is affected
29
what are the effects of atherosclerosis
- decreased blood supply to tissue/organ (ischaemia) - complete occlusion of the blood vessels lead to infarction - thrombosis - embolism
30
how does atherosclerosis cause ischaemia
narrowing of the blood vessel | lack of oxygen and nutrients going to the tissues
31
how does atherosclerosis cause infarction
if no blood can go through the blood vessel then it will lead to cell death
32
how does atherosclerosis cause thrombosis
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
what is an embolism
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
how is chronic periodonitits a risk factor for atherosclerosis
the pathogenic biofilm with bacteria can enter the blood stream
35
what is included in peripheral vascular disease
- ischaemia - claudication - gangrene - coagulation necrosis and infarction
36
what is claudication
a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.
37
what is gangrene
localized death and decomposition of body tissue, resulting from obstructed circulation or bacterial infection.
38
what is an aneurysm
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
what can cause an aneurysm
a number of factors such as developmental, degenerative or traumatic factors (eg infections)
40
what does AAA stand for and what is it
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
what are acute coronary conditions
- angina pectoris | - myocardial infarction
42
what is angina pectoris
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
how can you treat angina pectoris
medication and rest
44
what does infarction mean
loss / obstruction of the blood supply to an organ or region of tissue
45
what is myocardial infarction
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
why is anaerobic respiration ineffective a cause of myocardial infarction
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
how does the body try to heal a myocardial infarction
replacement of the dead muscle with fibrous tissue | fibrous tissue wont have the same function so the heart cannot return to normal
48
what happens histologically in coagulation necrosis
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
what does the process of healing involve in coagulation necrosis
``` 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
what are examples of chronic coronary syndromes
- congestive heart failure (usually follows IHD, hypertension or valvular heart disease) - ventricular hypertrophy - oedema - chronic venous congestion (CVC) of lung and liver
51
what is the pathophysiology of chronic coronary syndromes
- 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
what is apoptosis
programmed cell death
53
what are tumours of the blood vessels
- hamartomas - kaposi sarcoma - angiosarcoma (rare and aggressive)
54
where would you find a textbook haemangioma
new born infants have a large raised fleshy swelling when born very soft and can bleed quickly
55
what is a haemangioma
- 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
what are vascular malformations
- 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
what are the types of vascular malformations
- capillary - cavernous - struge weber syndrome
58
where are cavernous haemangioma common
midline of face | follows distribution of nerves
59
what is the struge weber syndrome haemangioma / vascular malformation
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
what is a kaposi sarcoma
- 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
what is angiosarcoma
- rare - aggressive cancer - malignant endothelial cells
62
what are cardiac tumours
- 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
how can valvular heart disease develop
can be congenital or acquired | acquired may be a result of other cardiac diseases such as ventricular hypertrophy
64
valvular heart disease pathology of the valves result in
- 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
what is calcific aortic stenosis
- 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
what results from rheumatic fever
rheumatic heart disease
67
what happens in rheumatic heart disease
- 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
what is infective endocarditis
microbial infection of heart valves
69
what are susceptible to infective endocarditis
damaged or prosthetic valves
70
what can cause infective endocarditis
oral pathogens > Streptococcus viridens > staphylococci aureus Found in mouth due to bad oral hygiene
71
what do vegetations found on the cusps in infective endocarditis contain
fibrin inflammatory cells infective pathogen
72
what can infective endocarditis cause
Can cause infective emboli | problems in other organs in other parts of the body
73
who does leanne kiss on the daily?
ben scott, heres his snapchat incase you forgot ;) ben0scott0

BDS2 - cardiovascular medicine (2 decks)

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