Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

brs (phase 1b) > (cardioresp) coronary heart disease & atherosclerosis > Flashcards

(cardioresp) coronary heart disease & atherosclerosis Flashcards

1
Q

how can risk factors be categorised?

A

modifiable risk factors

non-modifiable risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the modifiable risk factors for atherosclerosis?

A

smoking

lipids intake

blood pressure

diabetes

obesity

sedentary lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the non-modifiable risk factors for atherosclerosis?

A

age

sex

genetic background

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how can the risk factor of smoking be addressed and modified?

A

smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how can the risk factor of lipid intake be addressed and modified?

A

antihyperlipidaemic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how can the risk factor of blood pressure be addressed and modified?

A

use ABCD

A = ACE inhibitors
B = Beta-blockers
(better for younger patients under 55 and ‘non-black’ patients)

C = Calcium channel blockers
D = Diuretics
(better for older patients and ‘black’ patients of all age)

= prescribed in such a way that if two are needed, another from the opposite group is prescribed e.g. A and C // B and D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how can the risk factor of diabetes be addressed and modified?

A

dietary advice, weight loss & lifestyle modifications

gastric surgery to achieve weight loss

metformin, sulphonylureas, insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how can the risk factor of obesity be addressed and modified?

A

increased exercise + lifestyle modifications

obesity can increase the risk of hyperlipidaemia, hypertension, diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how can the risk factor of sedentary lifestyle be addressed and modified?

A

adopt a more active lifestyle w more exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

explain risk factor multiplication

A

risk factors are multiplicative when they are combined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how has the epidemiology of coronary heart disease changed over the years and what does this indicate?

A

people are getting CHD much later

more people are dying of CHD but at a higher age

= people are living longer AND treatment has improved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which improvements in treatment have contributed to the changes in CHD epidemiology?

A

people get CHD later and live longer with it

positives
= reduced hyperlipidaemia (statin treatment)
= reduced hypertension (antihypertensive treatment)

negatives
= increased obesity so increased diabetes

miscellaneous
= new improvements in diabetes treatment have doubtful effect on macrovascular disease
= changing pathology of coronary thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which areas are most affected by atherosclerosis?

A

coronary arteries

cerebral arteries

carotid arteries (tends to occur at the carotid bifurcations)

iliac arteries (at the aortic bifurcations)

coronary tree (supplying the myocardium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

at which bifurcations is atherosclerosis likely?

A

carotid bifurcation

aortic bifurcation

coronary tree (supplying the myocardium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does atherosclerosis occur at branches and bends?

i.e. bifurcations

A

areas of low shear stress and disturbed, turbulent blood flow (vortices)

= low shear stress is pro-inflammatory, pro-thrombotic and stimulates SMC proliferation and reduced NO production

= collective contributes to the growth of the atherosclerotic lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe the structure of the artery and its constituent layers

A

tunica intima (interna) = endothelium - subendothelium = internal elastic lamina

tunica media = smooth muscle cells

tunica adventitia = vasa vasorum, nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe the layers of tunica intima

A

endothelium

subendothelium (i.e. subendothelial space)

internal elastic lamina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does the tunic media consist of?

A

smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the tunic adventitia consist of?

A

vasa vasorum, nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where does the atherosclerotic plaque develop?

A

in the subendothelial space

i.e. subintimal space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where do low-density lipoproteins deposit in the arterial wall and why?

A

deposit in the subintimal/subendothelial space and bind to the matrix proteoglycans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why do arterial walls have a high amount of muscle?

A

to maintain and resist blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why do arterial walls have a high amount of elastic?

A

to cope w the pulsatile pressure and stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the function of the arterial endothelium?

A

separates the tissue walls from the blood

controls the vasodilation and vasoconstriction and therefore the blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the names of the six stages of atherosclerosis progression?
coronary artery at lesion-prone location type II lesion (fatty streak) type III (preatheroma) type IV (atheroma) type V (fibroatheroma) type VI (complicated lesion)
26
explain how an atherosclerotic plaque develops, from start to finish
1) endothelial damage due to hypertension/hyperglycaemia/hyperlipidaemia/smoking etc) 2) macrophages and LDL deposit in the subendothelial space; latter combines with free radicals from macrophages and forms oxLDL 3) oxLDL stimulates more macrophages to enter subendothelial space and engulf them 4) macrophages eventually engulf too many oxLDL molecules, leading to lipid overload and subsequent death (small pools of lipid) 5) as more macrophages die, more oxLDL & dead material accumulates to form extracellular lipid core 6) chemical signals released during lipid core formation cause SMC migration to wall off the lesion from the lumen (fibrous thickening) 7) complicated lesion = fibrous cap fissures/ruptures due to stress on endothelial wall and the atherosclerotic plaque components are exposed to the arterial blood leading to thrombogenesis
27
what is a type II lesion and what key event characterises this step in atherosclerosis?
type II lesion = fatty streak formation = macrophage foam cell formation (oxLDL is ingested by macrophages that subsequently form foam cells)
28
what is a type III lesion and what key event characterises this step in atherosclerosis?
type III lesion = preatheroma some foam cells die due to lipid overload and release their lipid contents = forming small extracellular pools of lipid
29
what is a type IV lesion and what key event characterises this step in atherosclerosis?
type IV lesion = atheroma most/all foam cells die due to lipid overload and multiple small pool os lipid coalesce to form a large lipid core
30
what is a type V lesion and what key event characterises this step in atherosclerosis?
type V lesion = fibroatheroma smooth muscle cells migrate to the luminal surface of the lipid core and form a fibrous cap (fibrous thickening!) = barrier bw atherosclerotic plaque and arterial blood
31
what is a type VI lesion and what key event characterises this step in atherosclerosis?
type VI lesion = complicated lesion rupture of atherosclerotic plaque due to damage to fibrous cap (fissure, hematoma, thrombus) = release of plaque contents into blood stimulating thrombogenesis
32
what is the main growth mechanism of atherosclerosis from type I to type IV lesions?
growth due to lipid addition
33
what is the main growth mechanism of atherosclerosis from type V to type VI lesions?
type V = smooth muscle and collagen increase type VI = thrombus formation or haematoma
34
when is the window of opportunity for primary prevention?
intermediate and advanced lesions
35
what forms of primary prevention occur in the intermediate-advanced lesion stage??
Life-style changes | Risk factor management
36
what are two complications that can occur as a result of atherosclerosis?
stenosis plaque rupture (due to occlusion of an artery = subsequent ischaemia, infarction OR due to extensive growth of lipid cores)
37
what clinical interventions are carried out in the complicated lesion stage of atherosclerosis?
secondary prevention catheter based interventions revascularisation surgery treatment of heart failure
38
name the 5 main cells involved in atherosclerosis
vascular endothelial cells monocyte-macrophages vascular smooth muscle cells platelets T lymphocytes
39
what are the two main functions of vascular endothelial cells in atherosclerosis?
1) barrier function (e.g. against LDL) 2) leukocyte recruitment (also involved in blood pressure control)
40
what are the main functions of monocyte-macrophages in atherosclerosis?
1) foam cell formation 2) release free radicals and metalloproteinases 3) release inflammatory cytokines and growth factors
41
what are the main functions of vascular smooth muscle cells in atherosclerosis?
1) migration, proliferation and formation of the fibrous cap (remodelling) 2) collagen synthesis
42
what are the main functions of platelets in atherosclerosis?
thrombus generation 3) release inflammatory cytokines and growth factors
43
what are the main functions of T lymohocytess in atherosclerosis?
activate macrophages
44
explain how fibrous cap thickness in atherosclerosis can cause either unstable angina or myocardial infarction
if fibrous cap is thick = plaque is stable, can narrow lumen BUT does not stop blood flow (unstable angina) BUT if thin capped = atherosclerotic plaques are thought to be more prone to rupture into lumen, blocking blood flow leading to thrombus formation (myocardial infarction)
45
differentiate between a thrombus and an embolus
thrombus = blood clot that forms in a vein embolus = usually part of a blood clot that has chipped off, that moves through the blood vessels until it reaches a vessel that is too small to let it pass
46
define thromboembolism
an embolus that breaks off a thrombus (blood clot)
47
what are MACEs?
major adverse cardiovascular events
48
which type of treatment during clinical trials resulted in fewer major adverse cardiovascular events (MACE)?
(CANTOS trial) = anti-IL1 antibody
49
why is IL-1 significant to the pathogenesis of atherosclerosis?
cholesterol crystals trigger macrophage/inflammatory cells of plaque to release more IL-1
50
which CD macrophage protein is appears brown-dyed?
CD68
51
why is foam cell debris (i.e. atherosclerotic plaque) dangerous?
contains toxic, thrombogenic molecules that can cause thrombus formation on exposure to blood
52
what is the main inflammatory cell of atherosclerosis?
macrophages, derived from blood monocytes
53
how are macrophage subtypes regulated?
combinations of transcription factors binding to regulatory sequences on DNA
54
what are the two types of macrophages?
inflammatory macrophages | resident macrophages
55
what is the function of inflammatory macrophages?
phagocytose pathogens
56
what is the function of resident macrophages?
maintain normal homeostatic mechanisms + suppress inflammatory activity
57
give examples of three types of resident macrophages
lung alveolar macrophages osteoclasts reticuloendothelial macrophages
58
what is the function of alveolar macrophages?
take up lung surfactant + reduce lung surface tension
59
what is the function of osteoclast macrophages?
bone resorption to regulate serum calcium levels
60
what is the function of reticuloendothelial macrophages?
iron homeostasis by recycling old, damaged erythrocytes
61
what can inflammation of the spleen lead to?
anaemia = due to impaired iron homeostasis
62
what is the function of LDL and where is it found?
synthesised in the liver = carries cholesterol from liver to rest of the body including arteries
63
what is the function of HDL?
synthesised in the liver/small intestine carries cholesterol from ‘peripheral tissues’ including arteries back to liver = reverse cholesterol transport
64
what is the function of oxLDL and where is it found?
found in vessel wall = highly inflammatory and toxic forms of LDL which forms due to action of free radicals on LDL (released by active macrophages)
65
where is cholesterol abnormally deposited?
in the arterial intima
66
what are the docking molecules of lipoproteins that assist with lipid binding?
apoproteins
67
what are contained within LDL micelles?
cholesterol esters
68
what is the fate of LDL cholesterol within the sub-endothelial space?
binds to matrix proteoglycans and forms a cholesterol-proteoglycan complex = at a greater risk of modification
69
what extracellular matrix protein binds to LDL cholesterol in the sub-endothelial space?
matrix proteoglycans
70
how does proteoglycan-cholesterol binding influence oxidation?
increases susceptibility to modification
71
how is the proteoglycan-cholesterol complex modified?
modified by free radicals released by activated macrophages
72
what is the fate of the modified LDL?
phagocytosis by macrophages leading to foam cell formation
73
what is familial hyperlipidaemia?
autosomal dominant condition that presents w massively elevated serum cholesterol levels
74
what are cholesterol levels in familial hyperlipidaemia?
approx >20 mmol/L | much higher than normal levels of 1-5 mmol/L
75
why does familial hyperlipidaemia occur?
defect/mutation of the LDL receptor of hepatocytes = failure to clear LDL from the blood
76
how does familial hyperlipidaemia present?
xanthomas (yellow plaques) increased number of atherosclerotic plaques
77
explain the pathophysiology of familial hyperlipidaemia
genetic mutation causes defect in LDL receptor on hepatocyte surface 1) reduced uptake of serum cholesterol into hepatocytes = reduced cellular cholesterol concentration = reduced inhibition of HMG-CoA reductase = increased cholesterol synthesis = further increases serum cholesterol levels
78
which cell structure has impaired functioning in FH?
LDL receptor of hepatocytes
79
what is the LDL receptor responsible for?
stimulates endocytosis of cholesterol and subsequent reduction in cellular cholesterol synthesis
80
which enzyme is inhibited due to increased uptake of extracellular cholesterol and what is the implication of this?
HMG-CoA reductase (key in cholesterol biosynthesis) = reduced cellular cholesterol biosynthesis
81
which receptors are sensitive to extracellular serum cholesterol?
LDL cholesterol
82
what can be deduced by the fact that in LDL-R negative patients, macrophages still continue to accumulate cholesterol?
macrophages, in atherosclerotic plaques, have a secondary LDL receptor! = takes up oxLDL ('scavenger receptor')
83
in which cells does cholesterol synthesis occur?
hepatocytes
84
on which cells are LDLRs found?
hepatocytes
85
what are the two effects of an LDL receptor mutation?
1) reduced sensitivity to serum cholesterol levels | 2) reduced inhibition of cellular cholesterol synthesis
86
true of false: LDLs are characterised by the presence of a lipid bilayer?
false | = lipid monolayer!
87
why are extremely high levels of HDL cholesterol harmful?
extremely high levels of HDL will promote CVD instead | above 2.5 mmol/L
88
how are macrophage scavenger receptors different to LDL receptors?
scavenger = not under negative feedback, take up oxLDL LDL = under negative feedback, take up LDL
89
what are the two types of macrophage scavenger receptors?
macrophage scavenger receptor A macrophage scavenger receptor B
90
what is another term for macrophage scavenger receptor A?
MSR-A | = CD204
91
what is another term for macrophage scavenger receptor A?
MSR-B | = CD36
92
what does MSR-A bind to?
oxidised LDL dead cells gram-positive bacteria (e.g. Staphylococcus, Streptococcus)
93
what does MSR-B bind to?
oxidised LDL dead cells malarial parasites
94
what are the two fates of oxLDL once it is taken up by macrophages?
1) stimulates inflammation | 2) modified and returned to HDL to be transported back into the liver via reverse cholesterol transport

brs (phase 1b) (71 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions