Clinical Aspects of Cardiovascular Risk Flashcards

1
Q

Most common cause of premature death?

A

Coronary Heart Disease - particularly in men

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

How does deprivation affect CVD risk?

A

Increased deprivation causes increased CVD risk

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

Reasons why CHD is the leading cause of death in the world?

A

Increased in no. of older people

Changes in underlying health habits, such as:
Increase in smoking
Dietary changes - increased cholesterol
Sedentary lifestyle
Rises in BP

Medical care focus on treatment rather than prevention

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

What is atherosclerosis?

A

Progressive disease characterised by plaque build-up within the arteries, which can partially/totally block the blood flow through as artery

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

Constituents of atherosclerotic plaque?

A

Formed from fatty substances, like cholesterol, cellular waste, calcium and fibrin. There is also inflammatory cell build-up

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

Complications of atherosclerotic plaque?

A

Bleeding into the plaque
Formation of a clot on the surface of the clot

If either happens and blocks the artery, an MI or stroke may result

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

Steps in atherosclerotic pathway?

A

Endothelial damage

Protective response - results in production of cellular adhesion molecules, such as cytokines, chemokines and growth factors

Monocytes and T lymphocytes attach to “sticky” surface of endothelial cells

Migrate through arterial wall to sub-endothelial space

Monocytes differentiate into macrophages take up oxidised LDL-C

Lipid-rich foam cells form the fatty streak and plaque

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

Causes of endothelial damage?

A

Haemodynamic forces (shear stress caused by e.g: hypertension)

Vasoactive substances

Mediators (cytokines) from blood cells

Cigarette smoke

Atherogenic diet

Elevated glucose levels

Oxidised LDL-C

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

What is atherothrombosis?

A

Formation of an acute thrombus in a vessel affected by atherosclerosis

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

Progression of atherothrombosis?

A

Initiated by changes in the vessel wall resulting from plaque disruption

Atherosclerotic plaque can become unstable and rupture, exposing components such as collagen to allow platelets to adhere to the damaged area and initiate thrombus formation

Thrombus can extend and occlude the vessel, leading to ischaemia and tissue injury

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

Risk factors for CVD?

A
Age 
Family history and ethnicity
Hypertension
Heart disease
Diabetes 
Smoking
Obesity
Unhealthy diet (atherogenic)
Oral contraception
Previous strokes/TIA
Binge drinking and substance abuse
Inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Modifiable risk factors for CVD?

A
Smoking
Dyslipidaemia: raised LDL, low HDL or raised triglycerides
Raised BP
Diabetes mellitus
Obesity
Dietary factors
Thrombogenic factors
Lack of exercise
Excess alcohol consumption

?Deprivation

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

Non-modifiable risk factors for CVD?

A

Personal history of CHD
Family history of CHD
Age
Gender

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

5 major classes of lipoproteins and functions?

A

Chylomicrons (largest) - synthesised in the gut after a fatty meal; transport dietary triglycerides from the gut to the sites of use and storage and are cleared rapidly from the bloodstream

VLDL (smaller than chylomicrons) - produced in the liver and are main carriers of endogenous (synthesised in the liver) triglycerides and cholesterol to sites of use/storage

IDL - formed during VLDL and chylomicron breakdown; involved in recycling of cholesterol by the liver, as well as formation of LDL in the blood. Also, implicated in atherogenesis

LDL - principal lipoproteins involved in atherosclerosis; OXIDISED LDL is the MOST ATHEROGENIC FORM as they are the main carriers of cholesterol

HDL (smallest) - return cholesterol from peripheral tissue to the liver, for excretion; protective against atherosclerosis

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

General rule for function of lipoproteins related to their size?

A

Smaller VLDL, IDL and LDL are all atherogenic
Large VLDL and chylomicrons are not

HDL carries cholesterol away from the arterial wall and is protective

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

LDL is more strongly associated with CHD events in which gender?

A

Males

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

Describe triglyceride involvement with CHD?

A

Increased risk of CHD events - may be related to low HDL levels and highly atherogenic forms of LDL cholesterol

18
Q

Factors that lower HDL levels?

A

Smoking
Obesity
Physical inactivity

19
Q

What do statins achieve?

A

Reduce CHD end points, by reducing total and LDL cholesterol

Other actions:
Improvement of endothelial dysfunction
Increased NO bioavailability
Anti-oxidant properties
Inhibition of inflammatory responses
Stabilisation of atherosclerotic plaques
20
Q

Why does familial hyperlipidaemia tend to occur?

A

Endogenous problem: genetic fault with LDL receptors

21
Q

What is xanthelasma?

A

Xanthomas of eyelids, may or may not be associated with hyperlipidaemia

Are fatty depositis

22
Q

What are tendon xanthomas?

A

Diffuse infiltration of tendon by lipids, e.g: extensor tendons of fingers, elbows, Achilles tendon (on of the MOST COMMON sites)

23
Q

What are tuberous xanthomas?

A

Lipid deposits in the dermis and subcutis; can be papuler, nodular or plaques

Located on extensor surfaces of large joints, hands, buttocks, heels and flexures

24
Q

What are eruptive xanthomas?

A

Small reddish-rellow papules on buttocks, posterior thighs of body folds

Tends to be associated with HIGH TRIGLYCERIDE LEVELS

25
Q

Diseases attributable to hypertension?

A
Heart failure
Left ventricular hypertrophy
MI
Hypertensive encephalopathy
CHD
Cerebral haemmorhage
Stroke
Chronic Kidney Failure
Blindness
Aortic aneurysm
Gangrene of the lower extremities
26
Q

Types of hypertension?

A

Essential hypertension - no underlying cause (90% of causes)

Secondary hypertension - underlying cause

27
Q

Hypertension treatment reduces?

A

Ischaemic heart disease
Stroke
Mortality

28
Q

Lifestyle modification?

A
Lose weight, if overweight
Limit alcohol intake
Increase physical activity
Reduce salt intake
Stop smoking
Limit intake of foods rich in fats and cholesterol
29
Q

Other risk factors that hypertensives have?

A
A large majority of hypertensive patients have other CV risk factors:
Dyslipidaemia
Diabetes
Age
Male gender
Smoking
Family history
30
Q

Greatest drop in BP is seen when?

A

With combination of BP lowering medications

31
Q

Reasons why type 2 diabetes mellitus predisposes to CVD?

A

It is associated with hypertension, abnormalities in lipoprotein metabolism and increased propensity to oxidative stress and endothelial dysfunction

Hyperglycaemia may accelerate vascular damage

Type 2 diabetes is also a hyper-coagulable state, with enhanced coagulation, decreased fibrinolysis and platelet aggregability

32
Q

What is the “ticking clock” hypothesis?

A

There are microvascular complication at onset of hyperglycaemia
There are macrovascular complications before the diagnosis of hyperglycaemia (pre-diabetes)

33
Q

What is the cornerstone of treatment?

A

Diet
Calorie intake to normalise weight

Plus or minus an exercise program

34
Q

Obesity increased risks of what events/issues?

A
Stroke
Angina
MI
Hypertension
Type 2 diabetes - risk of this with obese women is higher than for obese men
35
Q

What is the metabolic syndrome?

A

Metabolic syndrome is the medical term for a combination of hypercholesterolaemia/dyslipidaemia, diabetes, high blood pressure and obesity

36
Q

What is CRP and hs-CRP?

A

CRP - a non-specific, but very sensitive, inflammatory marker tested all the time

37
Q

Ethnic differences with CHD death rates?

A

South Asians living in the UK have a higher death rate - higher in women than men

Black Caribbean and Black Africans have a much lower CHD death rate than is average (lower in women than in men) - but much higher risk of stroke

38
Q

How to calculate CVD risk?

A
Assign score which takes into account:
Current age
Sex
SCOTTISH postcode
Family history
Diabetes
Cigarettes smoked daily
Systolic BP
Total cholesterol
HDL cholesterol
39
Q

What happens when risk factors co-exist?

A

For most CHD patients, they have multiple risk factors - when they co-exist, the sum of theit combined effect is much greater than the sum of their individual effects

40
Q

What is involved when, with treatment, ischaemia is the target?

A

Antianginal Medications:
Calcium Blockers
Nitrates
Beta Blockers

Revascularization:
Angioplasty
CABG

Risk factor modification

41
Q

What is involved when, with treatment, atherothrombosis is the target?

A
Aspirin
Statin
Beta Blocker
ACE Inhibitor
Exercise
Smoking Cessation

Symptom control:
Antianginal medications
Revascularization (smaller participation)