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Bio: Explain how each of these risk factors can influence the onset of CHD?
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zarahh09
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#1
Explain how each of these risk factors can influence the onset of CHD:
- High cholesterol
- Smoking
- Diet
I did this long back in 1st year and I barely remember anything to answer this question
- High cholesterol
- Smoking
- Diet
I did this long back in 1st year and I barely remember anything to answer this question
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Jpw1097
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#2
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#2
(Original post by zarahh09)
Explain how each of these risk factors can influence the onset of CHD:
- High cholesterol
- Smoking
- Diet
I did this long back in 1st year and I barely remember anything to answer this question
Explain how each of these risk factors can influence the onset of CHD:
- High cholesterol
- Smoking
- Diet
I did this long back in 1st year and I barely remember anything to answer this question
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zarahh09
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#3
(Original post by Jpw1097)
What sort of detail do you need? Clearly high cholesterol, smoking and poor diet will increase your risk of CHD, do you need to be able to explain why? In which case the question is how does high cholesterol, smoking and poor diet influence atherosclerosis.
What sort of detail do you need? Clearly high cholesterol, smoking and poor diet will increase your risk of CHD, do you need to be able to explain why? In which case the question is how does high cholesterol, smoking and poor diet influence atherosclerosis.
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macpatgh-Sheldon
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#4
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#4
Your Q appears to concentrate on the effect of these factors on ONSET of CHD.
[I] High cholesterol is likely to bring forward any ischaemic changes i.e. they are likely to occur earlier than in a person with normal cholesterol level. Other factors that are relevant are:-
a) How high the level is: a cholesterol level of 6 or so mmol/L might play a part [in conjunction with other risk factors] to bring e.g. angina pectoris or even an MI occurring a few years earlier
WHEREAS:
a very high cholesterol as in familial hypercholesterolaemia can result in family members as well the patient dying of MI very young e,g, in their 30s or 40s.
b) The balance between HDL cholesterol and LDL + VLDL cholesterol will have a distinct bearing: HDL is protective against CHD, whereas high LDL is a risk factor.
[II] Smoking is one of the most powerful drivers of atherosclerosis and ischaemic heart disease - I have come across patients who smoked heavily who died of MI in their early thirties. You can google the mechanisms of this disastrous effect.
[III] A diet high in unsaturated fats is perhaps even beneficial, while one high in saturated fats is deleterious - certain foods tend to increase e.g. cholesterol levels and others to reduce them - again the effect on "onset" is difficult to isolate or quantify for a single risk factor since all the relevant factors act jointly and over years.
When a clinician takes a history from a patient who e.g. presents with chest pain suggestive of myocardial ischaemia or worse, all these 3 and other factors need to be asked about, and a global clinical decision made together with findings of physical examination and special investigations.
I hope this gives you points to investigate further.
M
BTW thanks for the rep on your other Q!
[I] High cholesterol is likely to bring forward any ischaemic changes i.e. they are likely to occur earlier than in a person with normal cholesterol level. Other factors that are relevant are:-
a) How high the level is: a cholesterol level of 6 or so mmol/L might play a part [in conjunction with other risk factors] to bring e.g. angina pectoris or even an MI occurring a few years earlier
WHEREAS:
a very high cholesterol as in familial hypercholesterolaemia can result in family members as well the patient dying of MI very young e,g, in their 30s or 40s.
b) The balance between HDL cholesterol and LDL + VLDL cholesterol will have a distinct bearing: HDL is protective against CHD, whereas high LDL is a risk factor.
[II] Smoking is one of the most powerful drivers of atherosclerosis and ischaemic heart disease - I have come across patients who smoked heavily who died of MI in their early thirties. You can google the mechanisms of this disastrous effect.
[III] A diet high in unsaturated fats is perhaps even beneficial, while one high in saturated fats is deleterious - certain foods tend to increase e.g. cholesterol levels and others to reduce them - again the effect on "onset" is difficult to isolate or quantify for a single risk factor since all the relevant factors act jointly and over years.
When a clinician takes a history from a patient who e.g. presents with chest pain suggestive of myocardial ischaemia or worse, all these 3 and other factors need to be asked about, and a global clinical decision made together with findings of physical examination and special investigations.
I hope this gives you points to investigate further.
M
BTW thanks for the rep on your other Q!
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username5839543
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#5
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#5
(Original post by macpatgh-Sheldon)
Your Q appears to concentrate on the effect of these factors on ONSET of CHD.
[I] High cholesterol is likely to bring forward any ischaemic changes i.e. they are likely to occur earlier than in a person with normal cholesterol level. Other factors that are relevant are:-
a) How high the level is: a cholesterol level of 6 or so mmol/L might play a part [in conjunction with other risk factors] to bring e.g. angina pectoris or even an MI occurring a few years earlier
WHEREAS:
a very high cholesterol as in familial hypercholesterolaemia can result in family members as well the patient dying of MI very young e,g, in their 30s or 40s.
b) The balance between HDL cholesterol and LDL + VLDL cholesterol will have a distinct bearing: HDL is protective against CHD, whereas high LDL is a risk factor.
[II] Smoking is one of the most powerful drivers of atherosclerosis and ischaemic heart disease - I have come across patients who smoked heavily who died of MI in their early thirties. You can google the mechanisms of this disastrous effect.
[III] A diet high in unsaturated fats is perhaps even beneficial, while one high in saturated fats is deleterious - certain foods tend to increase e.g. cholesterol levels and others to reduce them - again the effect on "onset" is difficult to isolate or quantify for a single risk factor since all the relevant factors act jointly and over years.
When a clinician takes a history from a patient who e.g. presents with chest pain suggestive of myocardial ischaemia or worse, all these 3 and other factors need to be asked about, and a global clinical decision made together with findings of physical examination and special investigations.
I hope this gives you points to investigate further.
M
BTW thanks for the rep on your other Q!
Your Q appears to concentrate on the effect of these factors on ONSET of CHD.
[I] High cholesterol is likely to bring forward any ischaemic changes i.e. they are likely to occur earlier than in a person with normal cholesterol level. Other factors that are relevant are:-
a) How high the level is: a cholesterol level of 6 or so mmol/L might play a part [in conjunction with other risk factors] to bring e.g. angina pectoris or even an MI occurring a few years earlier
WHEREAS:
a very high cholesterol as in familial hypercholesterolaemia can result in family members as well the patient dying of MI very young e,g, in their 30s or 40s.
b) The balance between HDL cholesterol and LDL + VLDL cholesterol will have a distinct bearing: HDL is protective against CHD, whereas high LDL is a risk factor.
[II] Smoking is one of the most powerful drivers of atherosclerosis and ischaemic heart disease - I have come across patients who smoked heavily who died of MI in their early thirties. You can google the mechanisms of this disastrous effect.
[III] A diet high in unsaturated fats is perhaps even beneficial, while one high in saturated fats is deleterious - certain foods tend to increase e.g. cholesterol levels and others to reduce them - again the effect on "onset" is difficult to isolate or quantify for a single risk factor since all the relevant factors act jointly and over years.
When a clinician takes a history from a patient who e.g. presents with chest pain suggestive of myocardial ischaemia or worse, all these 3 and other factors need to be asked about, and a global clinical decision made together with findings of physical examination and special investigations.
I hope this gives you points to investigate further.
M
BTW thanks for the rep on your other Q!
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zarahh09
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#6
(Original post by Cancelled Alice)
Ayyyyy… that’s not the spirit, this person couldn’t be bothered to use google, do you think that it’s realistic that they will investigate the things that you’ve talked about further?
Ayyyyy… that’s not the spirit, this person couldn’t be bothered to use google, do you think that it’s realistic that they will investigate the things that you’ve talked about further?
I was going through the powerpoints from last year's lesson and this question was on it but we never did it in class
This is web is to ask for help not to just go to people's post to say DO IT YOURSELF
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Jpw1097
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#7
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#7
(Original post by zarahh09)
Like how each one increases the risk of CHD
Like how each one increases the risk of CHD
When there is injury to the vascular endothelium (the innermost layer of arterial walls), cholesterol or more precisely, LDL (which binds cholesterol), enters the arterial wall and is deposited in the tunica intima. It is this LDL which stimulates macrophages and stimulates the pro-inflammatory response. Atherosclerosis is an inflammatory process - it involves the recruitment of inflammatory immune cells to the tunica intima, it is not just the deposition of fat in the arterial wall.
Smoking contains lots of toxins which are irritants and cause injury to the vascular endothelium - this allows LDL to enter the tunica intima promoting atherosclerosis as above.
Finally, poor diet can promote atherosclerosis in a variety of ways. A diet high in fat (there is some controversy regarding saturated vs unsaturated fats) increases levels of LDL/cholesterol, some foods contain irritants which will cause endothelial injury. Fruit and vegetables contain antioxidants which helps to neutralise the pro-inflammatory process within the tunica intima.
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